PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32800545-6	2020	Ectopic overexpression of miR-206 has dramatically restricted the cell proliferation, glucose consumption and lactate production in CRC cells, whereas transfection of miR-206 inhibitor exhibited the opposite results.	Lactic Acid	110-117	microRNA 206	Homo sapiens	26-33
33803124-0	2021	Palmitic Acid Impairs Myogenesis and Alters Temporal Expression of miR-133a and miR-206 in C2C12 Myoblasts.	Palmitic Acid	0-13	microRNA 206	Homo sapiens	80-87
33803124-3	2021	Forty-eight hours of 100 microM PA induced a reduction of myotube diameter and increased the number of type I fibers, which was associated with increased miR-206 expression.	Palmitic Acid	32-34	microRNA 206	Homo sapiens	154-161
33803124-5	2021	Compared to control cells, 150 microM PA reduces myoblast proliferation and the expression of MyoD and miR-206 and miR-133a expression, leading to a reduced number and diameter of myotubes.	Palmitic Acid	38-40	microRNA 206	Homo sapiens	103-110
33803124-6	2021	PA (100 microM), despite not affecting proliferation, impairs myotube formation by reducing the expression of Myf5 and miR-206 and decreasing protein synthesis.	Palmitic Acid	0-2	microRNA 206	Homo sapiens	119-126
34746018-0	2021	LncRNA OTUD6B-AS1 Induces Cisplatin Resistance in Cervical Cancer Cells Through Up-Regulating Cyclin D2 via miR-206.	Cisplatin	26-35	microRNA 206	Homo sapiens	108-115
34746018-5	2021	Our qRT-PCR assays verified that miR-206 levels were down-regulated in cisplatin-resistant cervical cancer cells.	Cisplatin	71-80	microRNA 206	Homo sapiens	33-40
34746018-6	2021	The introduction of miR-206 sensitized cisplatin-resistant cervical cancer cells to cisplatin.	Cisplatin	39-48	microRNA 206	Homo sapiens	20-27
34746018-6	2021	The introduction of miR-206 sensitized cisplatin-resistant cervical cancer cells to cisplatin.	Cisplatin	84-93	microRNA 206	Homo sapiens	20-27
34746018-12	2021	Taken together, these results suggest that OTUD6B-AS1-mediated down-regulation of miR-206 increases CCND2 expression, leading to cisplatin resistance.	Cisplatin	129-138	microRNA 206	Homo sapiens	82-89
34697590-0	2021	Propranolol Suppresses Proliferation and Migration of HUVECs through Regulation of the miR-206/VEGFA Axis.	Propranolol	0-11	microRNA 206	Homo sapiens	87-94
34697590-8	2021	It was observed that propranolol induced the upregulation of miR-206 in HUVECs, which was caused by demethylation of the miR-206 promoter.	Propranolol	21-32	microRNA 206	Homo sapiens	61-68
34697590-8	2021	It was observed that propranolol induced the upregulation of miR-206 in HUVECs, which was caused by demethylation of the miR-206 promoter.	Propranolol	21-32	microRNA 206	Homo sapiens	121-128
34697590-9	2021	Moreover, propranolol significantly inhibited the proliferation of HUVECs by inducing apoptosis, while these phenomena were reversed by miR-206 antagomir.	Propranolol	10-21	microRNA 206	Homo sapiens	136-143
34697590-11	2021	In addition, propranolol notably inhibited the migration and induced G1 arrest of the HUVECs, whereas these results were eliminated by miR-206 antagomir.	Propranolol	13-24	microRNA 206	Homo sapiens	135-142
34697590-12	2021	Collectively, the findings of the present study demonstrated that propranolol may inhibit the proliferation and migration in HUVECs via modulating the miR-206/VEGFA axis.	Propranolol	66-77	microRNA 206	Homo sapiens	151-158
34196215-4	2021	The interaction between Linc1749808 and microRNA-206 (miR-206) was assessed by bioinformatic analysis and luciferase assays.	linc1749808	24-35	microRNA 206	Homo sapiens	40-52
34196215-4	2021	The interaction between Linc1749808 and microRNA-206 (miR-206) was assessed by bioinformatic analysis and luciferase assays.	linc1749808	24-35	microRNA 206	Homo sapiens	54-61
34196215-9	2021	Furthermore, Linc1749808 was found to act as a sponge of miR-206.	linc1749808	13-24	microRNA 206	Homo sapiens	57-64
34196215-10	2021	Inhibition of miR-206 counteracted the effect of Linc1749808 knockdown in 97H cells by regulating YAP1 and epithelial-mesenchymal transition (EMT).	linc1749808	49-60	microRNA 206	Homo sapiens	14-21
34196215-11	2021	In summary, these findings show that Linc1749808 can exacerbate the metastasis of HCC by sponging miR-206.	linc1749808	37-48	microRNA 206	Homo sapiens	98-105
35591763-0	2022	MicroRNA-206 inhibition and activation of the AMPK/Nampt signalling pathway enhance sevoflurane post-conditioning-induced amelioration of myocardial ischaemia/reperfusion injury.	Sevoflurane	84-95	microRNA 206	Homo sapiens	0-12
34975317-0	2022	MiR-206 suppresses the deterioration of intrahepatic cholangiocarcinoma and promotes sensitivity to chemotherapy by inhibiting interactions with stromal CAFs.	cafs	153-157	microRNA 206	Homo sapiens	0-7
33955799-0	2021	miR-1/133a and miR-206/133b clusters overcome HGF induced gefitinib resistance in non-small cell lung cancers with EGFR sensitive mutations.	Gefitinib	58-67	microRNA 206	Homo sapiens	15-27
33955799-5	2021	miR-1/133a and miR-206/133b clusters could overcome HGF induced gefitinib resistance.	Gefitinib	64-73	microRNA 206	Homo sapiens	15-22
33955799-9	2021	In conclusion, miR-1/133a and miR-206/133b clusters are able to exhibit the synergetic effect on overcoming HGF-induced gefitinib resistance in NSCLC and the mechanisms are through targeting multiple genes related to gefitinib resistance.	Gefitinib	120-129	microRNA 206	Homo sapiens	30-37
33955799-9	2021	In conclusion, miR-1/133a and miR-206/133b clusters are able to exhibit the synergetic effect on overcoming HGF-induced gefitinib resistance in NSCLC and the mechanisms are through targeting multiple genes related to gefitinib resistance.	Gefitinib	217-226	microRNA 206	Homo sapiens	30-37
33461610-7	2021	The effects of miR-206 on cell proliferation and cell apoptosis of hFOBs were measured by CCK-8 assay and flow cytometry, respectively.	hfobs	67-72	microRNA 206	Homo sapiens	15-22
33154668-0	2020	CircRAD18 Accelerates the Progression of Acute Myeloid Leukemia by Modulation of miR-206/PRKACB Axis.	circrad18	0-9	microRNA 206	Homo sapiens	81-88
34338434-0	2021	Astragalus polysaccharide ameliorates steroid-induced osteonecrosis of femoral head through miR-206/HIF-1alpha/BNIP3 axis.	Steroids	38-45	microRNA 206	Homo sapiens	92-99
34338434-2	2021	Here, we showed that astragalus polysaccharide (APS) improved femoral head necrosis via regulation of cell autophagy and apoptosis through microRNA (miR)-206/hypoxia inducible factor-1 (HIF-1alpha)/BCL2 interacting protein 3 (BNIP3) axis.	2-(chloromethyl)-4-(4-nitrophenyl)-1,3-thiazole	21-46	microRNA 206	Homo sapiens	139-157
34830882-8	2021	Serum microRNA-206 is a potential biomarker for colon (decreased) and breast (increased) cancer to monitor the disease evolution and the effects promoted by the AET.	beta-Aminoethyl Isothiourea	161-164	microRNA 206	Homo sapiens	6-18
34147072-6	2021	RESULTS: High expression of miR-206 was positively correlated with peripheral Th17/Treg imbalance in patients with OA.	th17	78-82	microRNA 206	Homo sapiens	28-35
34147072-6	2021	RESULTS: High expression of miR-206 was positively correlated with peripheral Th17/Treg imbalance in patients with OA.	treg	83-87	microRNA 206	Homo sapiens	28-35
34147072-9	2021	In vivo assay demonstrated that antagomiR directed against miR-206 restored Th17/Treg balance during the development of OA.	treg	81-85	microRNA 206	Homo sapiens	59-66
34147072-10	2021	CONCLUSION: MiR-206 contributed to the progression of OA by modulating Th17/Treg imbalance, suggesting that miR-206 inhibition might be a promising therapeutic strategy for the treatment of OA.	treg	76-80	microRNA 206	Homo sapiens	12-19
35489671-8	2022	Taken together, these results demonstrate the role of circTmeff-1 in the reconsolidation of cocaine-associated memory and that circTmeff-1 may function as a decoy for miR-206 to regulate the expression of BDNF.	Cocaine	92-99	microRNA 206	Homo sapiens	167-174
35304514-9	2022	MiR-206 is reported to be down-regulated in Luminal-A type of breast cancer.	Phenobarbital	44-51	microRNA 206	Homo sapiens	0-7
33945508-0	2021	Epithelial microRNA-206 targets CD39/extracellular ATP to upregulate airway IL-25 and TSLP in type 2-high asthma.	Adenosine Triphosphate	51-54	microRNA 206	Homo sapiens	11-23
33945508-5	2021	CD39, an ectonucleotidase degrading ATP, was a target of miR-206 and upregulated in asthma.	Adenosine Triphosphate	36-39	microRNA 206	Homo sapiens	57-64
33945508-6	2021	Allergen-induced acute extracellular ATP accumulation led to miR-206 downregulation and CD39 upregulation in human bronchial epithelial cells, forming a feedback loop to eliminate excessive ATP.	Adenosine Triphosphate	37-40	microRNA 206	Homo sapiens	61-68
33945508-6	2021	Allergen-induced acute extracellular ATP accumulation led to miR-206 downregulation and CD39 upregulation in human bronchial epithelial cells, forming a feedback loop to eliminate excessive ATP.	Adenosine Triphosphate	190-193	microRNA 206	Homo sapiens	61-68
33452572-0	2021	Ursolic acid ameliorates Nthy-ori 3-1 cells injury induced by IL-1beta through limiting MALAT1/miR-206/PTGS1 ceRNA network and NF-kappaB signaling pathway.	ursolic acid	0-12	microRNA 206	Homo sapiens	95-102
33452572-13	2021	However, UA ameliorated the Nthy-ori 3-1 cells injury induced by IL-1beta through mediating the MALAT1/miR-206/PTGS1 ceRNA network and NF-kappaB signaling pathway.	ursolic acid	9-11	microRNA 206	Homo sapiens	103-110
33452572-14	2021	CONCLUSIONS: UA treatment significantly relieved the injury of Nthy-ori 3-1 cells via inhibiting the ceRNA mechanism of MALAT1/miR-206/PTGS1 and inflammatory pathways, insinuating that UA may be helpful for the treatment of AIT.	ursolic acid	13-15	microRNA 206	Homo sapiens	127-134
33086901-6	2021	RESULTS: Based on microarray analyses, we found that microRNA-206 may be involved in asthma induced PAH stimulated by PM2.5.	[4-(3-AMINOMETHYL-PHENYL)-PIPERIDIN-1-YL]-(5-PHENETHYL- PYRIDIN-3-YL)-METHANONE	118-121	microRNA 206	Homo sapiens	53-65
33292230-0	2020	miR-206 as a prognostic and sensitivity biomarker for platinum chemotherapy in epithelial ovarian cancer.	Platinum	54-62	microRNA 206	Homo sapiens	0-7
33292230-2	2020	We found a subset of miRNAs associated with the response to first-line platinum-based chemotherapy in EOC by microarray, and miR-206 was one of the most significant miRNAs.	Platinum	71-79	microRNA 206	Homo sapiens	125-132
33292230-3	2020	The purposes of this study were to evaluate the prognostic and platinum-resistance predictive value of miR-206 in EOC patients and to investigate the functional roles of miR-206 in regulating the platinum resistance of EOC and the underlying mechanism.	Platinum	196-204	microRNA 206	Homo sapiens	170-177
33292230-11	2020	High miR-206 expression was related to poor prognosis in EOC patients who received platinum-based chemotherapy and predicted chemoresistance to platinum treatment.	Platinum	83-91	microRNA 206	Homo sapiens	5-12
33292230-11	2020	High miR-206 expression was related to poor prognosis in EOC patients who received platinum-based chemotherapy and predicted chemoresistance to platinum treatment.	Platinum	144-152	microRNA 206	Homo sapiens	5-12
33292230-12	2020	Overexpression of miR-206 in cisplatin-sensitive EOC cell lines significantly increased cell viability, migration and invasion in the presence of cisplatin and decreased cisplatin-induced apoptosis.	Cisplatin	29-38	microRNA 206	Homo sapiens	18-25
33292230-12	2020	Overexpression of miR-206 in cisplatin-sensitive EOC cell lines significantly increased cell viability, migration and invasion in the presence of cisplatin and decreased cisplatin-induced apoptosis.	Cisplatin	146-155	microRNA 206	Homo sapiens	18-25
33292230-12	2020	Overexpression of miR-206 in cisplatin-sensitive EOC cell lines significantly increased cell viability, migration and invasion in the presence of cisplatin and decreased cisplatin-induced apoptosis.	Cisplatin	146-155	microRNA 206	Homo sapiens	18-25
33292230-13	2020	Cx43, a target gene of miR-206, was negatively regulated by miR-206 in EOC cell lines and significantly related to better prognosis in patients who received platinum-based chemotherapy (KmPlot).	Platinum	157-165	microRNA 206	Homo sapiens	23-30
33292230-13	2020	Cx43, a target gene of miR-206, was negatively regulated by miR-206 in EOC cell lines and significantly related to better prognosis in patients who received platinum-based chemotherapy (KmPlot).	Platinum	157-165	microRNA 206	Homo sapiens	60-67
33292230-14	2020	miR-206 had high expression and Cx43 had low expression in platinum-sensitive EOC cell lines compared with resistant ones.	Platinum	59-67	microRNA 206	Homo sapiens	0-7
32074070-0	2020	Curcumin inhibits migration and invasion of non-small cell lung cancer cells through up-regulation of miR-206 and suppression of PI3K/AKT/mTOR signaling pathway.	Curcumin	0-8	microRNA 206	Homo sapiens	102-109
32700168-0	2020	Ghrelin promotes the osteogenic differentiation of rMSCs via miR-206 and the ERK1/2 pathway.	Ghrelin	0-7	microRNA 206	Homo sapiens	61-68
32700168-6	2020	RESULTS: Ghrelin inhibited the expression of miR-206 to promote the osteogenic differentiation of rMSCs.	Ghrelin	9-16	microRNA 206	Homo sapiens	45-52
32700168-7	2020	Moreover, ghrelin increased the phosphorylation of ERK1/2, while overexpression of miR-206 suppressed ERK1/2 phosphorylation, indicating that miR-206 can regulate the ERK1/2 pathway.	Ghrelin	10-17	microRNA 206	Homo sapiens	142-149
32700168-9	2020	CONCLUSIONS: Ghrelin promotes the osteogenic differentiation of rMSCs via miR-206 and the ERK1/2 pathway.	Ghrelin	13-20	microRNA 206	Homo sapiens	74-81
32700168-4	2020	In the present study, the function of miR-206 in the ghrelin-mediated osteogenic differentiation of rabbit bone marrow-derived mesenchymal stromal cells (rMSCs) was explored.	Ghrelin	53-60	microRNA 206	Homo sapiens	38-45
32074070-3	2020	In this study, we investigated the involvement of miR-206 in curcumin"s anti-invasion and anti-migration in NSCLC.	Curcumin	61-69	microRNA 206	Homo sapiens	50-57
32074070-8	2020	Curcumin significantly inhibited migration and invasion in A549 cells, accompanied by significantly elevated miR-206 expression.	Curcumin	0-8	microRNA 206	Homo sapiens	109-116
32074070-11	2020	Furthermore, miR-206 mimics improved the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT in A549 cells.	Curcumin	63-71	microRNA 206	Homo sapiens	13-20
32074070-12	2020	On the contrary, MiR-206 inhibitors reversed the inhibitory effects of curcumin on cell migration, invasion and the phosphorylation level of mTOR and AKT.	Curcumin	71-79	microRNA 206	Homo sapiens	17-24
32074070-13	2020	In conclusion, curcumin inhibited cell invasion and migration in NSCLC by elevating the expression of miR-206 which further suppressed the activation of the PI3K/AKT/mTOR pathway.	Curcumin	15-23	microRNA 206	Homo sapiens	102-109
32509200-0	2020	Quercetin stimulates osteogenic differentiation of bone marrow stromal cells through miRNA-206/connexin 43 pathway.	Quercetin	0-9	microRNA 206	Homo sapiens	85-94
32509200-9	2020	In the presence of agomir of miR-206, effects of quercetin on mineralization, alkaline phosphatase activity and osteoblast-specific genes expression were suppressed.	Quercetin	49-58	microRNA 206	Homo sapiens	29-36
32509200-10	2020	Most of all, Cx43 protein level was also blocked while overexpression of miR-206 against quercetin effects.	Quercetin	89-98	microRNA 206	Homo sapiens	73-80
32509200-12	2020	The osteogenic effect of quercetin is partly modulated through miR-206/Cx43 pathway.	Quercetin	25-34	microRNA 206	Homo sapiens	63-70
32036213-8	2020	Three miRNAs, including let-7b-5p, miR-206 and miR-486-5p, were verified to be significantly and steadily increased in heroin abusers, and miR-9-3p was significantly increased in MA abusers compared with normal controls.	Heroin	119-125	microRNA 206	Homo sapiens	35-42
31408569-10	2019	The intracellular accumulation of estrone-3-sulphate was reduced by 30% in cells overexpressing miR-206.	estrone sulfate	34-52	microRNA 206	Homo sapiens	96-103
31749176-5	2020	The present study demonstrated that hsa-miR-27b-3p, hsa-miR-151a-5p and hsa-miR-206 play an important role in the effects of l-carnitine treatment of the spermatozoa in asthenospermia patients.	Carnitine	125-136	microRNA 206	Homo sapiens	72-83
31749176-7	2020	The results show that the target mRNAs of hsa-miR-206 may change the activity of ATP synthase and participate in the cAMP signalling pathway and the calcium signalling pathway, which may play an important role in sperm motility.	Adenosine Triphosphate	81-84	microRNA 206	Homo sapiens	42-53
31749176-7	2020	The results show that the target mRNAs of hsa-miR-206 may change the activity of ATP synthase and participate in the cAMP signalling pathway and the calcium signalling pathway, which may play an important role in sperm motility.	Cyclic AMP	117-121	microRNA 206	Homo sapiens	42-53
31749176-7	2020	The results show that the target mRNAs of hsa-miR-206 may change the activity of ATP synthase and participate in the cAMP signalling pathway and the calcium signalling pathway, which may play an important role in sperm motility.	Calcium	149-156	microRNA 206	Homo sapiens	42-53
32021281-0	2020	Propofol Inhibits the Migration and Invasion of Glioma Cells by Blocking the PI3K/AKT Pathway Through miR-206/ROCK1 Axis.	Propofol	0-8	microRNA 206	Homo sapiens	102-109
32021281-8	2020	MiR-206 was decreased in glioma tissues and cells, while propofol exposure induced the upregulation of miR-206 in glioma cells.	Propofol	57-65	microRNA 206	Homo sapiens	103-110
32021281-9	2020	Besides that, we also found overexpressed miR-206 enhanced propofol-mediated inhibition on the migration, invasion, and PI3K/AKT pathway activation of glioma cells.	Propofol	59-67	microRNA 206	Homo sapiens	42-49
32021281-12	2020	The rescue assay indicated that the miR-206/ROCK1 axis was involved in propofol-induced inhibition on the migration, invasion, and PI3K/AKT pathway activation in glioma cells.	Propofol	71-79	microRNA 206	Homo sapiens	36-43
32021281-13	2020	Conclusion: Propofol inhibited the migration and invasion of glioma cells by blocking the PI3K/AKT pathway through the miR-206/ROCK1 axis, suggesting an effective clinical implication for the anesthetic to prevent the metastasis of glioma.	Propofol	12-20	microRNA 206	Homo sapiens	119-126
31880296-0	2019	miR-206 Inhibits Cell Proliferation and Extracellular Matrix Accumulation by Targeting Hypoxia-Inducible Factor 1-alpha (HIF-1alpha) in Mesangial Cells Treated with High Glucose.	Glucose	170-177	microRNA 206	Homo sapiens	0-7
31880296-1	2019	BACKGROUND The goal of this study was to investigate the expression of miR-206 in human glomerular mesangial cells (hMCs) treated by exposure to high glucose (HG) levels, to assess the influence of miR-206 on the proliferation and extracellular matrix (ECM) deposition of hMCs, and to investigate the potential mechanisms of action.	Glucose	150-157	microRNA 206	Homo sapiens	71-78
31742336-12	2020	Furthermore, miR-206 reduced glucose uptake, lactate production and ATP generation in NSCLC cells via HK2 repression.	Glucose	29-36	microRNA 206	Homo sapiens	13-20
31742336-12	2020	Furthermore, miR-206 reduced glucose uptake, lactate production and ATP generation in NSCLC cells via HK2 repression.	Lactic Acid	45-52	microRNA 206	Homo sapiens	13-20
31742336-12	2020	Furthermore, miR-206 reduced glucose uptake, lactate production and ATP generation in NSCLC cells via HK2 repression.	Adenosine Triphosphate	68-71	microRNA 206	Homo sapiens	13-20
31163553-13	2019	Further MTT assay indicated that inhibiting miR-206 attenuated the suppressing effect of si-FOXD2-AS1 on the proliferation of TU686 cells.	monooxyethylene trimethylolpropane tristearate	8-11	microRNA 206	Homo sapiens	44-51
31507089-0	2019	Reciprocal regulation of miR-206 and IL-6/STAT3 pathway mediates IL6-induced gefitinib resistance in EGFR-mutant lung cancer cells.	Gefitinib	77-86	microRNA 206	Homo sapiens	25-32
31507089-4	2019	In this study, we investigated the role of miR-206 in IL6-induced gefitinib-resistant EGFR-mutated lung cancer cell lines.	Gefitinib	66-75	microRNA 206	Homo sapiens	43-50
31507089-5	2019	We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway.	Gefitinib	50-59	microRNA 206	Homo sapiens	22-29
31507089-5	2019	We showed that forced miR-206 expression restored gefitinib sensitivity in IL6-induced gefitinib-resistant EGFR-mutant lung cancer cells by inhibiting IL6/JAK1/STAT3 pathway.	Gefitinib	87-96	microRNA 206	Homo sapiens	22-29
31507089-8	2019	Taken together, our findings reveal a direct role of miR-206 in regulating IL-6/STAT3 pathway and contrarily activated IL-6/STAT3 signalling mediates the miR-206 maturation process in gefitinib-resistant EGFR-mutant lung cancer cells.	Gefitinib	184-193	microRNA 206	Homo sapiens	53-60
31507089-8	2019	Taken together, our findings reveal a direct role of miR-206 in regulating IL-6/STAT3 pathway and contrarily activated IL-6/STAT3 signalling mediates the miR-206 maturation process in gefitinib-resistant EGFR-mutant lung cancer cells.	Gefitinib	184-193	microRNA 206	Homo sapiens	154-161
31571906-14	2019	Furthermore, Met is the target gene of miR-206 in experimental cells.	methionylmethionine	13-16	microRNA 206	Homo sapiens	39-46
31571906-15	2019	The suppression on these signaling pathways was acted by targeting miR-206/Met axis.	methionylmethionine	75-78	microRNA 206	Homo sapiens	67-74
31571906-17	2019	Furthermore, si-circZFR suppressed Wnt/beta-catenin and PI3K/AKT pathways via targeting miR-206/Met axis.	methionylmethionine	96-99	microRNA 206	Homo sapiens	88-95
30982495-0	2019	PPARbeta/delta Agonist GW501516 Inhibits Tumorigenesis and Promotes Apoptosis of the Undifferentiated Nasopharyngeal Carcinoma C666-1 Cells by Regulating miR-206.	GW 501516	23-31	microRNA 206	Homo sapiens	154-161
30982495-3	2019	Among the assayed miRNAs that were involved in regulating the expression of antiapoptotic protein Bcl-2, miR-206 was increased significantly and specifically by GW501516 in C666-1 cells at both the in vitro level and at the in vivo xenograft samples.	GW 501516	161-169	microRNA 206	Homo sapiens	105-112
30982495-4	2019	The induction on miR-206 expression caused by GW501516 was capable of being antagonized by the PPARbeta/delta antagonist GSK3787 and AMPK antagonist dorsomorphin in C666-1 cells.	GW 501516	46-54	microRNA 206	Homo sapiens	17-24
30982495-4	2019	The induction on miR-206 expression caused by GW501516 was capable of being antagonized by the PPARbeta/delta antagonist GSK3787 and AMPK antagonist dorsomorphin in C666-1 cells.	4-chloro-N-(2-((5-trifluoromethyl-2-pyridyl)sulfonyl)ethyl)benzamide	121-128	microRNA 206	Homo sapiens	17-24
30982495-4	2019	The induction on miR-206 expression caused by GW501516 was capable of being antagonized by the PPARbeta/delta antagonist GSK3787 and AMPK antagonist dorsomorphin in C666-1 cells.	dorsomorphin	149-161	microRNA 206	Homo sapiens	17-24
30982495-5	2019	GW501516"s suppression on the growth and apoptosis of C666-1 cells was found to be dependent on the presence of miR-206.	GW 501516	0-8	microRNA 206	Homo sapiens	112-119
30982495-9	2019	Taken together, the current data demonstrated that miR-206 plays a critical role in the direct apoptosis-promoting effect induced by GW501516 in C666-1 cells.	GW 501516	133-141	microRNA 206	Homo sapiens	51-58
30904818-11	2019	Besides, over-expression of miR-206 could notably promoted the expression of NIS, an intrinsic membrane protein that mediates the active transport of iodide into the thyroid and other tissues, playing a critical role in the progress.	Nickel	77-80	microRNA 206	Homo sapiens	28-35
30904818-11	2019	Besides, over-expression of miR-206 could notably promoted the expression of NIS, an intrinsic membrane protein that mediates the active transport of iodide into the thyroid and other tissues, playing a critical role in the progress.	Iodides	150-156	microRNA 206	Homo sapiens	28-35
30904818-15	2019	CONCLUSION: miR-206 contributed to euthyrox resistance in PTC cells through blockage p38 and JNK signaling pathway by targeting MAP4K3, providing a potential therapeutic application for the treatment of patients with euthyrox-resistant PTC in the further.	Thyroxine	35-43	microRNA 206	Homo sapiens	12-19
30904818-15	2019	CONCLUSION: miR-206 contributed to euthyrox resistance in PTC cells through blockage p38 and JNK signaling pathway by targeting MAP4K3, providing a potential therapeutic application for the treatment of patients with euthyrox-resistant PTC in the further.	Thyroxine	217-225	microRNA 206	Homo sapiens	12-19
30804229-6	2019	Furthermore, miR-206 overexpressing BMSCs showed attenuated alkaline phosphatase (ALP) activity, Alizarin Red staining, and osteocalcin secretion.	alizarin	97-109	microRNA 206	Homo sapiens	13-20
30804229-10	2019	Finally, restoration of GLS in miR-206 overexpressing BMSCs led to recovery of glutamine metabolism and osteogenic differentiation.	Glutamine	79-88	microRNA 206	Homo sapiens	31-38
30804229-11	2019	In summary, these results reveal a new insight into the mechanisms of the miR-206-mediated osteogenesis through regulating glutamine metabolism.	Glutamine	123-132	microRNA 206	Homo sapiens	74-81
30204869-0	2019	miR-206 as a Biomarker for Response to Mesalamine Treatment in Ulcerative Colitis.	Mesalamine	39-49	microRNA 206	Homo sapiens	0-7
30204869-4	2019	This study correlates expression levels of miR-206 with histologic remission in patients treated via long-term mesalamine treatment to identify a possible mode of action for this mainstay drug for UC.	Mesalamine	111-121	microRNA 206	Homo sapiens	43-50
30204869-5	2019	Methods: Expression of miR-206 and its target A3AR were analyzed in HT29 cell line before and after mesalamine treatment (2 mM) at different time points (0, 4, 12, and 24 hours) by qRT-PCR and western blot analysis.	Mesalamine	100-110	microRNA 206	Homo sapiens	23-30
30204869-7	2019	Results: miR-206 transcripts decreased 2.23-fold (P = 0.0001) 4 hours after 2 mM mesalamine treatment in HT29 colon cells compared with untreated controls.	Mesalamine	81-91	microRNA 206	Homo sapiens	9-16
30204869-9	2019	miR-206 relative expression decreased significantly in patients treated with 4.8 g of mesalamine (P = 0.002) but not with 2.4 g (P = 0.35).	Mesalamine	86-96	microRNA 206	Homo sapiens	0-7
30204869-10	2019	Tissue assessment of sequential mesalamine-treated colonoscopic biopsies indicate a strong correlation between downregulation of miR-206 and histologic improvement (R = 0.9111).	Mesalamine	32-42	microRNA 206	Homo sapiens	129-136
30204869-12	2019	Downregulation of miR-206 by long-term mesalamine treatment may confer a protective effect in inducing and maintaining histologic remission.	Mesalamine	39-49	microRNA 206	Homo sapiens	18-25
30204869-13	2019	Thus, miR-206 expression levels can be utilized as a possible biomarker for therapeutic response to mesalamine treatment.	Mesalamine	100-110	microRNA 206	Homo sapiens	6-13
29886033-12	2018	Targeting of NAMPT-mediated NAD salvage pathway by miR-206 might provide a new insight in the possible molecular mechanism of breast cancer cell growth regulation.	NAD	28-31	microRNA 206	Homo sapiens	51-58
30111166-3	2018	In the current work, we created miR-206-overexpressing cell lines (HT-1080, Caco2, iASC, and SS-iASC) using permanent transfection.	caco2	76-81	microRNA 206	Homo sapiens	32-39
30135139-0	2018	MiRNA-206 suppresses PGE2-induced colorectal cancer cell proliferation, migration, and invasion by targetting TM4SF1.	Dinoprostone	21-25	microRNA 206	Homo sapiens	0-9
30135139-2	2018	Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1).The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively.	Dinoprostone	53-69	microRNA 206	Homo sapiens	30-37
30135139-2	2018	Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1).The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively.	Dinoprostone	71-75	microRNA 206	Homo sapiens	30-37
30135139-2	2018	Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1).The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively.	Dinoprostone	245-249	microRNA 206	Homo sapiens	30-37
30135139-2	2018	Here, we investigated whether miR-206 is involved in prostaglandin E2 (PGE2)-induced epithelial-mesenchymal transition (EMT) in colorectal cancer (CRC) cells through the targetting of transmembrane 4 L six family member 1 (TM4SF1).The effect of PGE2 on growth and apoptosis of CRC cells was evaluated using the MTT assay and flow cytometry analysis, respectively.	monooxyethylene trimethylolpropane tristearate	311-314	microRNA 206	Homo sapiens	30-37
30135139-5	2018	A miR-206 or TM4SF1 construct was transfected into cells with PGE2.	Dinoprostone	62-66	microRNA 206	Homo sapiens	2-9
30135139-12	2018	Moreover, the overexpression of miR-206 decreased CRC cell proliferation, migration, and invasion compared with control group in PGE2-induced cells, and these effects could be recovered by the overexpression of TM4SF1.	Dinoprostone	129-133	microRNA 206	Homo sapiens	32-39
30135139-13	2018	Overexpression of miR-206 also suppressed the expression of beta-catenin, VEGF, MMP-9, Snail, and Vimentin and enhanced E-cadherin expression in PGE2-induced cells.	Dinoprostone	145-149	microRNA 206	Homo sapiens	18-25
29971911-0	2018	Long non-coding RNA FTH1P3 activates paclitaxel resistance in breast cancer through miR-206/ABCB1.	Paclitaxel	37-47	microRNA 206	Homo sapiens	84-91
29971911-8	2018	In summary, our results reveal the potential regulatory mechanism of FTH1P3 on breast cancer paclitaxel resistance through miR-206/ABCB1, providing a novel insight for the breast cancer chemoresistance.	Paclitaxel	93-103	microRNA 206	Homo sapiens	123-130
29886033-11	2018	miR-206 reduced NAMPT expression at the protein level, leading to a significant decrease in the intracellular NAD level and subsequent decline in cell survival and induction of apoptosis.	NAD	110-113	microRNA 206	Homo sapiens	0-7
29484422-10	2018	Inhibition of endogenous miR-206 expression decreased intracellular TG and TC content in HepG2 cells.	Triglycerides	68-70	microRNA 206	Homo sapiens	25-32
29664235-0	2018	miR-1-3p and miR-206 sensitizes HGF-induced gefitinib-resistant human lung cancer cells through inhibition of c-Met signalling and EMT.	Gefitinib	44-53	microRNA 206	Homo sapiens	13-20
29664235-4	2018	In this study, we showed that miR-1-3p and miR-206 restored the sensitivities of lung cancer cells PC-9 and HCC-827 to gefitinib in present of HGF.	Gefitinib	119-128	microRNA 206	Homo sapiens	43-50
29664235-6	2018	Knockdown of c-Met mimicked the effects of miR-1-3p and miR-206 transfections Meanwhile, c-Met overexpression attenuated the effects of miR-1-3p and miR-206 in HGF-induced gefitinib resistance of lung cancers.	Gefitinib	172-181	microRNA 206	Homo sapiens	56-63
29664235-6	2018	Knockdown of c-Met mimicked the effects of miR-1-3p and miR-206 transfections Meanwhile, c-Met overexpression attenuated the effects of miR-1-3p and miR-206 in HGF-induced gefitinib resistance of lung cancers.	Gefitinib	172-181	microRNA 206	Homo sapiens	149-156
29484422-10	2018	Inhibition of endogenous miR-206 expression decreased intracellular TG and TC content in HepG2 cells.	Technetium	75-77	microRNA 206	Homo sapiens	25-32
29484422-11	2018	By contrast, overexpression of miR-206 in HepG2 partially prevented the reduction in TG content induced by treatment with T3.	Triglycerides	85-87	microRNA 206	Homo sapiens	31-38
29115490-0	2018	MicroRNA-206 contributes to the progression of steroid-induced avascular necrosis of the femoral head by inducing osteoblast apoptosis by suppressing programmed cell death 4.	Steroids	47-54	microRNA 206	Homo sapiens	0-12
29636622-0	2018	miR-206 regulates 5-FU resistance by targeting Bcl-2 in colon cancer cells.	Fluorouracil	18-22	microRNA 206	Homo sapiens	0-7
29636622-3	2018	The current study aimed to explore the potential function of miR-206 in 5-FU resistance.	Fluorouracil	72-76	microRNA 206	Homo sapiens	61-68
29636622-5	2018	miR-206 mimic was transfected to 5-FU-FR CRC, and the 5-FU sensitivity was detected by MTS and flow cytometry.	Fluorouracil	33-37	microRNA 206	Homo sapiens	0-7
29636622-9	2018	We also identified miR-206 targeting Bcl-2 directly in CRC, which is required for miR-206 mediated-5-FU resistance.	Fluorouracil	99-103	microRNA 206	Homo sapiens	19-26
29636622-9	2018	We also identified miR-206 targeting Bcl-2 directly in CRC, which is required for miR-206 mediated-5-FU resistance.	Fluorouracil	99-103	microRNA 206	Homo sapiens	82-89
29483552-2	2018	TGF-beta1 reduced microRNA-206 (miR-206) level by activating Smad2/3, and this in turn up-regulated histone deacetylase 4 (HDAC4) and consequently increased cyclin D1 protein leading to ASMCs proliferation.	asmcs	186-191	microRNA 206	Homo sapiens	18-30
29483552-2	2018	TGF-beta1 reduced microRNA-206 (miR-206) level by activating Smad2/3, and this in turn up-regulated histone deacetylase 4 (HDAC4) and consequently increased cyclin D1 protein leading to ASMCs proliferation.	asmcs	186-191	microRNA 206	Homo sapiens	32-39
29523226-12	2018	Moreover, co-transfection of anti-miR-206 oligodeoxyribonucleotide (AMO-206) in cervical cancer cells reversed the effect of lncRNA UCA1 on VEGF.	Oligodeoxyribonucleotides	42-66	microRNA 206	Homo sapiens	34-41
29483552-5	2018	Our study suggests that activation of AMPK modulates miR-206/HDAC4/cyclin D1 signaling pathway, particularly targeting on HDAC4, to suppress ASMCs proliferation and therefore has a potential value in the prevention and treatment of asthma by alleviating airway remodeling.	asmcs	141-146	microRNA 206	Homo sapiens	53-60
29115490-1	2018	The expression of microRNA-206 (miR-206) is aberrantly induced in steroid-induced avascular necrosis of femoral head (SANFH).	Steroids	66-73	microRNA 206	Homo sapiens	18-30
29115490-1	2018	The expression of microRNA-206 (miR-206) is aberrantly induced in steroid-induced avascular necrosis of femoral head (SANFH).	Steroids	66-73	microRNA 206	Homo sapiens	32-39
29115490-5	2018	The level of miR-206 and PDCD4 was regulated in human osteoblast lineage hFOB1.19 and the effect of different treatments on cell viability, proliferation, apoptosis and differentiation potential of osteoblasts were analyzed with a Cell Counting kit-8, 5-ethynyl-2"-deoxyuridine staining, flow cytometry and Hoechst staining.	8, 5-ethynyl-2"-deoxyuridine	249-277	microRNA 206	Homo sapiens	13-20
29115490-5	2018	The level of miR-206 and PDCD4 was regulated in human osteoblast lineage hFOB1.19 and the effect of different treatments on cell viability, proliferation, apoptosis and differentiation potential of osteoblasts were analyzed with a Cell Counting kit-8, 5-ethynyl-2"-deoxyuridine staining, flow cytometry and Hoechst staining.	hoechst	307-314	microRNA 206	Homo sapiens	13-20
29115490-9	2018	Inhibiting the expression of miR-206 increased cell viability and proliferation but had no effect on cell apoptosis, as detected by flow cytometry and Hoechst staining.	hoechst	151-158	microRNA 206	Homo sapiens	29-36
29387248-4	2018	In the present study, whether miR-206 and SOX9 mediated cell apoptosis in dexamethasone (DEX)-induced LCPD was investigated.	Dexamethasone	74-87	microRNA 206	Homo sapiens	30-37
28834127-4	2018	Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels.	Vincristine	15-26	microRNA 206	Homo sapiens	129-136
28834127-4	2018	Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels.	Irinotecan	28-38	microRNA 206	Homo sapiens	129-136
29387248-4	2018	In the present study, whether miR-206 and SOX9 mediated cell apoptosis in dexamethasone (DEX)-induced LCPD was investigated.	Dexamethasone	89-92	microRNA 206	Homo sapiens	30-37
28834127-4	2018	Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels.	Temozolomide	44-56	microRNA 206	Homo sapiens	129-136
29387248-10	2018	miR-206 was overexpressed while SOX9 was downregulated in chondrocytes treated with DEX obtained from patients with LCPD.	Dexamethasone	84-87	microRNA 206	Homo sapiens	0-7
28987947-4	2017	The effect of miR-206 on cell proliferation was tested by MTT assay, colony formation and cell cycle assays.	monooxyethylene trimethylolpropane tristearate	58-61	microRNA 206	Homo sapiens	14-21
28834127-4	2018	Replacement of vincristine, irinotecan, and temozolomide (VIT) for VAC induced a marked tumor reduction and normalization of the miR-206 levels.	vit	58-61	microRNA 206	Homo sapiens	129-136
28869449-0	2017	Propofol-induced neurotoxicity in hESCs involved in activation of miR-206/PUMA signal pathway.	Propofol	0-8	microRNA 206	Homo sapiens	66-73
29104627-5	2017	It was demonstrated that the relative survival rate of VSMCs was suppressed by miR-206 compared with scramble controls.	vsmcs	55-60	microRNA 206	Homo sapiens	79-86
28637658-0	2017	Decreased myoblast differentiation in chronic binge alcohol-administered simian immunodeficiency virus-infected male macaques: role of decreased miR-206.	Alcohols	52-59	microRNA 206	Homo sapiens	145-152
28637658-11	2017	These results support a mechanistic role for decreased miR-206 in suppression of myoblast differentiation resulting from chronic alcohol and SIV infection.	Alcohols	129-136	microRNA 206	Homo sapiens	55-62
28869449-3	2017	A recent report found that propofol could significantly upregulat miR-206 expression in the human ASCs.	Propofol	27-35	microRNA 206	Homo sapiens	66-73
28869449-11	2017	RESULTS: hESCs exposed to propofol showed a significant increase in TUNEL positive cells and cleaved caspase-3 expression, followed by the upregulation of miR-206 and PUMA expression.	Propofol	26-34	microRNA 206	Homo sapiens	155-162
28869449-12	2017	Targeting PUMA inhibits propofol-induced cell apoptosis; miR-206 knockdown decreased propofol-induced cell apoptosis, cleaved caspase-3 and PUMA expression.	Propofol	85-93	microRNA 206	Homo sapiens	57-64
28869449-13	2017	CONCLUSIONS: Propofol induce s cell death in hESC-derived neurons via activation of miR-206/PUMA signal pathway.	Propofol	13-21	microRNA 206	Homo sapiens	84-91
28713273-7	2017	Interestingly, we found that the upregulation of 6PGD in cisplatin-resistant cells was due to the decreased expression of miR-206 and miR-613, which we found to target this enzyme.	Cisplatin	57-66	microRNA 206	Homo sapiens	122-129
28713273-8	2017	We further demonstrate that suppressing 6PGD using shRNA, inhibitor or miR-206/miR-613, either as single agents or in combination, could sensitize cisplatin-resistant cancer cells to cisplatin treatment and thereby improving the therapeutic efficacy of cisplatin.	Cisplatin	147-156	microRNA 206	Homo sapiens	71-78
28713273-8	2017	We further demonstrate that suppressing 6PGD using shRNA, inhibitor or miR-206/miR-613, either as single agents or in combination, could sensitize cisplatin-resistant cancer cells to cisplatin treatment and thereby improving the therapeutic efficacy of cisplatin.	Cisplatin	183-192	microRNA 206	Homo sapiens	71-78
28713273-8	2017	We further demonstrate that suppressing 6PGD using shRNA, inhibitor or miR-206/miR-613, either as single agents or in combination, could sensitize cisplatin-resistant cancer cells to cisplatin treatment and thereby improving the therapeutic efficacy of cisplatin.	Cisplatin	183-192	microRNA 206	Homo sapiens	71-78
28391353-12	2017	Functionally, miR-206 knockdown decreased tamoxifen sensitivity in tamoxifen-sensitive (TamS) MCF-7 cells, while miR-206 overexpression and WBP2 knockdown enhanced the sensitivity in tamoxifen-resistant (TamR) MCF-7 cells.	Tamoxifen	42-51	microRNA 206	Homo sapiens	14-21
28391353-12	2017	Functionally, miR-206 knockdown decreased tamoxifen sensitivity in tamoxifen-sensitive (TamS) MCF-7 cells, while miR-206 overexpression and WBP2 knockdown enhanced the sensitivity in tamoxifen-resistant (TamR) MCF-7 cells.	Tamoxifen	67-76	microRNA 206	Homo sapiens	14-21
28391353-12	2017	Functionally, miR-206 knockdown decreased tamoxifen sensitivity in tamoxifen-sensitive (TamS) MCF-7 cells, while miR-206 overexpression and WBP2 knockdown enhanced the sensitivity in tamoxifen-resistant (TamR) MCF-7 cells.	tams	88-92	microRNA 206	Homo sapiens	14-21
28391353-12	2017	Functionally, miR-206 knockdown decreased tamoxifen sensitivity in tamoxifen-sensitive (TamS) MCF-7 cells, while miR-206 overexpression and WBP2 knockdown enhanced the sensitivity in tamoxifen-resistant (TamR) MCF-7 cells.	Tamoxifen	67-76	microRNA 206	Homo sapiens	14-21
28391353-13	2017	CONCLUSION: Based on these findings, we infer that the miR-206/WBP2 axis can modulate tamoxifen sensitivity via regulating G1/S progression in ER+ breast cancer.	Tamoxifen	86-95	microRNA 206	Homo sapiens	55-62
27488535-6	2016	These effects were not mediated by altered myoD expression; instead, cells with elevated HO-1 produced less reactive oxygen species, resulting in nuclear localization of HDAC4 and miR-206 repression.	Reactive Oxygen Species	108-131	microRNA 206	Homo sapiens	180-187
27662297-8	2017	At the baseline, serum levels of miR-206 in aMCI-AD group were significantly elevated compared to aMCI-aMCI group and the same trend was found at 5-year follow-up time point as well.	amci-ad	44-51	microRNA 206	Homo sapiens	33-40
27662297-8	2017	At the baseline, serum levels of miR-206 in aMCI-AD group were significantly elevated compared to aMCI-aMCI group and the same trend was found at 5-year follow-up time point as well.	amci	44-48	microRNA 206	Homo sapiens	33-40
27662297-8	2017	At the baseline, serum levels of miR-206 in aMCI-AD group were significantly elevated compared to aMCI-aMCI group and the same trend was found at 5-year follow-up time point as well.	amci	98-102	microRNA 206	Homo sapiens	33-40
27662297-12	2017	These results suggested that increased serum miR-206 level might be a potential predictor of conversion from aMCI to AD.	amci	109-113	microRNA 206	Homo sapiens	45-52
28377359-5	2017	The effect of miR-206 on the sensitivity of ovarian cancer cells to 5-Fu was assessed.	Fluorouracil	68-72	microRNA 206	Homo sapiens	14-21
28377359-10	2017	Transfection of SKOV3 cells with miR-206 significantly lowered the IC50 of 5-Fu to enhance the chemotherapy sensitivity of the cells to 5-Fu.	Fluorouracil	75-79	microRNA 206	Homo sapiens	33-40
28377359-10	2017	Transfection of SKOV3 cells with miR-206 significantly lowered the IC50 of 5-Fu to enhance the chemotherapy sensitivity of the cells to 5-Fu.	Fluorouracil	136-140	microRNA 206	Homo sapiens	33-40
28377359-11	2017	CONCLUSION: As a potential tumor suppressor, miR-206 directly targets CDK4 to suppress the cell growth and enhance the chemotherapy sensitivity to 5-Fu in ovarian cancer cells in vitro.	Fluorouracil	147-151	microRNA 206	Homo sapiens	45-52
27893428-8	2017	Furthermore, miR-206 increased dextran sodium sulphate-induced colitis severity (i.e., increased bodyweight loss, DAI score, colon shrinkage, and MPO activity), which was partially ameliorated by miR-206-antagomir treatment.	dextran sodium sulphate	31-54	microRNA 206	Homo sapiens	196-203
27858746-7	2015	Steroid treatment reversed expression patterns of several microRNAs (miR-206, miR-181a, miR-4538, miR-4539, miR-606, and miR-454) that were altered in the young DMD patients.	Steroids	0-7	microRNA 206	Homo sapiens	69-76
27014910-0	2016	miR-206 regulates cisplatin resistance and EMT in human lung adenocarcinoma cells partly by targeting MET.	Cisplatin	18-27	microRNA 206	Homo sapiens	0-7
27014910-2	2016	The aims of this study were to explore the potential role of miR-206 in governing cisplatin resistance and EMT in lung cancer cells.	Cisplatin	82-91	microRNA 206	Homo sapiens	61-68
27014910-4	2016	Ectopic expression of miR-206 mimics inhibited cisplatin resistance, reversed the EMT phenotype, decreased the migration and invasion in these DDP-resistant cells.	Cisplatin	47-56	microRNA 206	Homo sapiens	22-29
27014910-5	2016	In contrast, miR-206 inhibitors increased cisplatin resistance, EMT, cell migration and invasion in non-DDP-resistant cells.	Cisplatin	42-51	microRNA 206	Homo sapiens	13-20
27014910-9	2016	In lung adenocarcinoma tissues, we demonstrated that low expression of miR-206 were also correlated with increased cisplatin resistance and MET expression.	Cisplatin	115-124	microRNA 206	Homo sapiens	71-78
27014910-10	2016	In addition, we revealed that miR-206 overexpression reduced cisplatin resistance and EMT in DDP-resistant cells, partly due to inactivation of MET/PI3K/AKT/mTOR signaling pathway, and subsequent downregulation of MDR1, ZEB1 and Snail expression.	Cisplatin	61-70	microRNA 206	Homo sapiens	30-37
27014910-12	2016	Taken together, our study implied that activation of miR-206 or inactivation of its target gene pathway could serve as a novel approach to reverse cisplatin resistance in lung adenocarcinomas cells.	Cisplatin	147-156	microRNA 206	Homo sapiens	53-60
27858746-9	2015	Since steroids decreased miR-206 expression to control levels, this could provide one mechanism by which steroids improve motor function.	Steroids	6-14	microRNA 206	Homo sapiens	25-32
27858746-9	2015	Since steroids decreased miR-206 expression to control levels, this could provide one mechanism by which steroids improve motor function.	Steroids	105-113	microRNA 206	Homo sapiens	25-32
26093295-8	2015	In addition, miR-206 overexpression impeded fructose-2,6-bisphosphate (F2,6BP) production, diminished lactate generation and reduced cell proliferation and migration in breast cancer cells.	fructose 2,6-diphosphate	44-69	microRNA 206	Homo sapiens	13-20
26325180-9	2015	In addition, miR-206 also decreased the gene expression of MMP-9, CCND1 and CCND2 while increased the gene expression of p57 (Kip2) in A549 and SK-MES-1 cells.	2-(N-morpholino)ethanesulfonic acid	147-150	microRNA 206	Homo sapiens	13-20
26153023-7	2015	Moreover, ARS treatment in ERMS cells ROS-dependently induces the expression of the myo-miRs, miR-133a and miR-206, which are down-regulated in RMS, and reduces PAX7 protein levels.	Reactive Oxygen Species	38-41	microRNA 206	Homo sapiens	107-114
26093295-5	2015	17beta-estradiol dose-dependently decreased miR-206 expression as well as enhanced PFKFB3 mRNA and protein expression in estrogen receptor alpha (ERalpha) positive breast cancer cells.	Estradiol	0-16	microRNA 206	Homo sapiens	44-51
26093295-8	2015	In addition, miR-206 overexpression impeded fructose-2,6-bisphosphate (F2,6BP) production, diminished lactate generation and reduced cell proliferation and migration in breast cancer cells.	fructose 2,6-diphosphate	71-77	microRNA 206	Homo sapiens	13-20
26093295-7	2015	miR-206 modulated PFKFB3 expression in MCF-7, T47D and SUM159 cells, which was influenced by 17beta-estradiol depending on ERalpha expression.	Estradiol	93-109	microRNA 206	Homo sapiens	0-7
26093295-8	2015	In addition, miR-206 overexpression impeded fructose-2,6-bisphosphate (F2,6BP) production, diminished lactate generation and reduced cell proliferation and migration in breast cancer cells.	Lactic Acid	102-109	microRNA 206	Homo sapiens	13-20
25644430-14	2015	As an alternative, we used DCA in combination with miR-206 to increase the flux of pyruvate into the mitochondrion by reactivating PDH.	Pyruvic Acid	83-91	microRNA 206	Homo sapiens	51-58
25644430-15	2015	DCA enhanced the inhibition of RMS cell growth induced by miR-206, and sustained it upon miR-206 de-induction.	Dichloroacetic Acid	0-3	microRNA 206	Homo sapiens	58-65
25644430-15	2015	DCA enhanced the inhibition of RMS cell growth induced by miR-206, and sustained it upon miR-206 de-induction.	Dichloroacetic Acid	0-3	microRNA 206	Homo sapiens	89-96
24603323-0	2014	miR-206 controls LXRalpha expression and promotes LXR-mediated cholesterol efflux in macrophages.	Cholesterol	63-74	microRNA 206	Homo sapiens	0-7
25202071-0	2014	Decreased miR-206 expression in BRCA1 wild-type triple-negative breast cancer cells after concomitant treatment with gemcitabine and a Poly(ADP-ribose) polymerase-1 inhibitor.	gemcitabine	117-128	microRNA 206	Homo sapiens	10-17
24919811-4	2014	miR-206 mimics were transiently transfected into HepG2 cells using Lipofectamine  2000.	Lipofectamine	67-86	microRNA 206	Homo sapiens	0-7
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	134-145	microRNA 206	Homo sapiens	90-97
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	134-145	microRNA 206	Homo sapiens	117-124
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	134-145	microRNA 206	Homo sapiens	117-124
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	209-220	microRNA 206	Homo sapiens	90-97
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	209-220	microRNA 206	Homo sapiens	117-124
24603323-10	2014	The physiological relevance of these findings was proven by gain- and loss-of-function of miR-206; overexpression of miR-206 enhanced cholesterol efflux in human macrophages and knocking out miR-206 decreased cholesterol efflux from MPMs.	Cholesterol	209-220	microRNA 206	Homo sapiens	117-124
17849003-7	2007	Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample.	Adenosine Monophosphate	175-178	microRNA 206	Homo sapiens	34-45
23858090-4	2013	Recent evidence suggests that the expression of muscle-specific miRNAs (myomirs), including miR-1, miR-133a/b, miR-206, and miR-499, is modulated by essential amino acid ingestion, endurance exercise, and endurance exercise training.	Amino Acids, Essential	149-169	microRNA 206	Homo sapiens	111-118
23628900-12	2013	Transfection of pre-miR miR-206 in hypoxic conditions led to increased expression of HIF-1alpha and Fhl-1 rather than abolishing hypoxia-induced HIF-1alpha and Fhl-1, as was expected, and promoted the entry of cells into the S phase and enhanced PASMC proliferation.	pasmc	246-251	microRNA 206	Homo sapiens	24-31
23628900-15	2013	In conclusion, hypoxia-induced downregulation of miR-206 promotes PH by targeting the HIF-1alpha/Fhl-1 pathway in PASMCs.	pasmcs	114-120	microRNA 206	Homo sapiens	49-56
23071643-8	2012	miR-206 expression in mouse PASMCs was correlated with an increase in right ventricular systolic pressure.	pasmcs	28-34	microRNA 206	Homo sapiens	0-7
20655308-0	2010	miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes.	Glucose	56-63	microRNA 206	Homo sapiens	6-13
20655308-2	2010	After stimulation of cardiomyocytes with high glucose in vivo and in vitro, significant up-regulation of miR-1/miR-206 and post-transcriptional modulation of Hsp 60 were observed.	Glucose	46-53	microRNA 206	Homo sapiens	111-118
20655308-5	2010	These results revealed that miR-1 and miR-206 regulate Hsp60 expression, contributing to high glucose-mediated apoptosis in cardiomyocytes.	Glucose	94-101	microRNA 206	Homo sapiens	38-45
19567520-12	2009	L-thyroxine therapy induced a large down-regulation of the primary transcripts of the noncoding microRNA pair miR-206/miR-133b.	Thyroxine	0-11	microRNA 206	Homo sapiens	110-117
24604205-10	2014	Further analysis revealed that 17beta-E2 treatment significantly promoted cellular proliferation and invasion of estrogen-dependent CAOV-3 and BG-1 cells, which could be reversed by the introduction of miR-206 mimics.	17beta-e2	31-40	microRNA 206	Homo sapiens	202-209
22508046-5	2012	Ectopic expression of miR-206 inhibited cell proliferation, and promoted cell apoptosis in U343 and SK-N-SH cell by using MTT, Edu Apollo assay and Flow cytometry analysis.	monooxyethylene trimethylolpropane tristearate	122-125	microRNA 206	Homo sapiens	22-29
21302623-6	2010	METHODS AND STUDY DESIGN: miR-206 mimics were transfected into MDA-MB-231 cells using LipofectamineTM 2000.	lipofectaminetm	86-101	microRNA 206	Homo sapiens	26-33
17849003-7	2007	Two SNPs rs17578796 and rs1700 in hsa-mir-206 (mir-206) and hsa-mit-198 (mir-198) showed nominal significant allelic association to schizophrenia in the Danish and Norwegian sample respectively (P = 0.0021 & p = 0.038), of which only rs17578796 was significant in the joint sample.	Adenosine Monophosphate	175-178	microRNA 206	Homo sapiens	38-45