PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32713345-15	2020	As a result, circPACRGL promoted CRC cell proliferation, migration and invasion, as well as differentiation of N1 to N2 neutrophils via miR-142-3p/miR-506-3p-TGF-beta1 axis.	circpacrgl	13-23	microRNA 506	Homo sapiens	147-154
34987126-3	2021	Stimulation of human intestinal epithelial cells (Caco-2) with 1000 muM of 5-ASA suppressed the levels of miR-125b, miR-150, miR-155, miR-346 and miR-506, which are known to be involved in the regulation of colitis and/or colorectal cancer in patients with inflammatory bowel disease.	Mesalamine	75-80	microRNA 506	Homo sapiens	146-153
35392987-0	2022	Knockdown of circ_0003928 ameliorates high glucose-induced dysfunction of human tubular epithelial cells through the miR-506-3p/HDAC4 pathway in diabetic nephropathy.	Glucose	43-50	microRNA 506	Homo sapiens	117-124
33666835-0	2021	Alginic acid inhibits non-small cell lung cancer-induced angiogenesis via activating miR-506 expression.	Alginic Acid	0-12	microRNA 506	Homo sapiens	85-92
33980925-8	2021	A functional in vitro analysis in Caco-2 cells showed that the induction of miR-506 activity by miR-506 mimic or GDCDA bile acid suppressed, whereas inhibition of miR-506 by miR-506 inhibitor or lipopolysaccharide (LPS) upregulated the expression of the examined target genes.	gdcda bile acid	113-128	microRNA 506	Homo sapiens	76-83
33980925-10	2021	In ascending colons with PSC + UC, upregulation of miR-506 may result in failure of bicarbonate secretion and inhibition of p53, which predisposes to pro-tumorigenic transformation.	Bicarbonates	84-95	microRNA 506	Homo sapiens	51-58
32833189-5	2021	The relationship between LINC01541 and miR-506-5p was verified in 17beta-E2-stimulated ESCs.	17beta-e2	66-75	microRNA 506	Homo sapiens	39-46
32833189-10	2021	Furthermore, silencing of miR-506-5p promoted apoptosis and suppressed the proliferation of 17beta-E2-treated ESCs.	17beta-e2	92-101	microRNA 506	Homo sapiens	26-33
34062009-10	2021	Moreover, we indicated that the ERK/Fos signaling pathway was intensively inactivated after overexpression of miR-506 and PENK both in vitro and in vivo, which was further validated by the ERK1/2-specific inhibitor SCH772984.	SCH772984	215-224	microRNA 506	Homo sapiens	110-117
33000204-0	2020	KCNQ1OT1 contributes to sorafenib resistance and programmed death-ligand-1-mediated immune escape via sponging miR-506 in hepatocellular carcinoma cells.	Sorafenib	24-33	microRNA 506	Homo sapiens	111-118
33000204-8	2020	KCNQ1OT1 and PD-L1 were found to be upregulated and miR-506 was downregulated in sorafenib-resistant HCC tissues and cells.	Sorafenib	81-90	microRNA 506	Homo sapiens	52-59
33000204-11	2020	In addition, it was demonstrated that KCNQ1OT1 functioned as a competing endogenous RNA of miR-506 and increased PD-L1 expression in sorafenib-resistant HCC cells.	Sorafenib	133-142	microRNA 506	Homo sapiens	91-98
33000204-12	2020	miR-506 inhibition abolished the effects of KCNQ1OT1 knockdown on sorafenib sensitivity, tumor growth, the tumor microenvironment and T-cell apoptosis.	Sorafenib	66-75	microRNA 506	Homo sapiens	0-7
33000204-13	2020	In conclusion, KCNQ1OT1 knockdown inhibited sorafenib resistance and PD-L1-mediated immune escape by sponging miR-506 in sorafenib-resistant HCC cells.	Sorafenib	121-130	microRNA 506	Homo sapiens	110-117
32944040-6	2020	Next, miR-506 was transfected with concentrations of 50 and 100 nM with Lipofectamine 2000.	Lipofectamine	72-90	microRNA 506	Homo sapiens	6-13
31087496-7	2019	Moreover, a further miRNAs screen by qRT-PCR indicated that miR-124-3p and miR-506-3p (miR-124/506) were remarkably reduced in sorafenib insensitive patients.	Sorafenib	127-136	microRNA 506	Homo sapiens	87-98
32099459-0	2019	circPCNX and Pecanex Promote Hepatocellular Carcinoma Cell Viability by Inhibiting miR-506.	circpcnx	0-8	microRNA 506	Homo sapiens	83-90
31515847-12	2019	TRPV1 channel stimulation and ROS generation, which was related to osteoclastogenesis, were reduced via miR-506 depletion.	Reactive Oxygen Species	30-33	microRNA 506	Homo sapiens	104-111
31515847-13	2019	miR-506 modulated osteoclastogenesis by targeting SIRT1 expression in part through modulation of the TRPV1 channel, ROS production, and TNF-alpha.	Reactive Oxygen Species	116-119	microRNA 506	Homo sapiens	0-7
31087496-9	2019	Interestingly, we finally proved that the sorafenib resistant cells regained sensitivity for sorafenib by EZH2 intervention with miR-124/506 overexpression or EZH2 inhibitor treatment in vitro and in vivo, which will lead to the decreased tri-methylation at lysine 27 of histone H3 (H3K27me3) and increased acetylated lysine 27 of histone H3 (H3K27ac) levels.	Sorafenib	42-51	microRNA 506	Homo sapiens	129-140
31087496-9	2019	Interestingly, we finally proved that the sorafenib resistant cells regained sensitivity for sorafenib by EZH2 intervention with miR-124/506 overexpression or EZH2 inhibitor treatment in vitro and in vivo, which will lead to the decreased tri-methylation at lysine 27 of histone H3 (H3K27me3) and increased acetylated lysine 27 of histone H3 (H3K27ac) levels.	Sorafenib	93-102	microRNA 506	Homo sapiens	129-140
31087496-9	2019	Interestingly, we finally proved that the sorafenib resistant cells regained sensitivity for sorafenib by EZH2 intervention with miR-124/506 overexpression or EZH2 inhibitor treatment in vitro and in vivo, which will lead to the decreased tri-methylation at lysine 27 of histone H3 (H3K27me3) and increased acetylated lysine 27 of histone H3 (H3K27ac) levels.	Lysine	258-264	microRNA 506	Homo sapiens	129-140
31087496-9	2019	Interestingly, we finally proved that the sorafenib resistant cells regained sensitivity for sorafenib by EZH2 intervention with miR-124/506 overexpression or EZH2 inhibitor treatment in vitro and in vivo, which will lead to the decreased tri-methylation at lysine 27 of histone H3 (H3K27me3) and increased acetylated lysine 27 of histone H3 (H3K27ac) levels.	Lysine	318-324	microRNA 506	Homo sapiens	129-140
30105876-6	2018	Moreover, DQ786243 reversed the inhibitory effect of miR-506 on the growth of ovarian cancer cells, which might be involved in the derepression of cAMP responsive element binding protein 1 (CREB1) expression.	dq786243	10-18	microRNA 506	Homo sapiens	53-60
30669957-8	2019	The alterations induced by miR-506-3p mimics were partly reversed by SPHK1 overexpression or treatment of rapamycin.	Sirolimus	106-115	microRNA 506	Homo sapiens	27-34
30105876-9	2018	Taken together, our study showed for the first time that DQ786243 interacted with miR-506 and promoted progression of ovarian cancer via targeting CREB1 in ovarian cancer.	dq786243	57-65	microRNA 506	Homo sapiens	82-89
28849090-9	2017	H2O2 markedly upregulated the expression levels of KLF4 and KLF5, and downregulated the expression levels of miR-506 and miR-124 in the HCMs.	Hydrogen Peroxide	0-4	microRNA 506	Homo sapiens	109-116
28922472-8	2018	In cholangiocytes, miR-506 (1) induced dedifferentiation with down-regulation of biliary and epithelial markers together with up-regulation of mesenchymal, proinflammatory, and profibrotic markers; (2) impaired cell proliferation and adhesion; (3) increased oxidative and endoplasmic reticulum stress; (4) caused DNA damage; and (5) sensitized to caspase-3-dependent apoptosis induced by cytotoxic bile acids.	Bile Acids and Salts	398-408	microRNA 506	Homo sapiens	19-26
28962898-4	2018	Recently, it has been shown that microRNA-506 (miR-506) on chromosome X is up-regulated in PBC cholangiocytes and suppresses AE2 expression, which sensitizes cholangiocytes to bile salt-induced apoptosis by activating soluble adenylyl cyclase (sAC), an evolutionarily conserved bicarbonate sensor.	Bile Acids and Salts	176-185	microRNA 506	Homo sapiens	33-45
28962898-4	2018	Recently, it has been shown that microRNA-506 (miR-506) on chromosome X is up-regulated in PBC cholangiocytes and suppresses AE2 expression, which sensitizes cholangiocytes to bile salt-induced apoptosis by activating soluble adenylyl cyclase (sAC), an evolutionarily conserved bicarbonate sensor.	Bile Acids and Salts	176-185	microRNA 506	Homo sapiens	47-54
28962898-4	2018	Recently, it has been shown that microRNA-506 (miR-506) on chromosome X is up-regulated in PBC cholangiocytes and suppresses AE2 expression, which sensitizes cholangiocytes to bile salt-induced apoptosis by activating soluble adenylyl cyclase (sAC), an evolutionarily conserved bicarbonate sensor.	Bicarbonates	278-289	microRNA 506	Homo sapiens	33-45
28962898-4	2018	Recently, it has been shown that microRNA-506 (miR-506) on chromosome X is up-regulated in PBC cholangiocytes and suppresses AE2 expression, which sensitizes cholangiocytes to bile salt-induced apoptosis by activating soluble adenylyl cyclase (sAC), an evolutionarily conserved bicarbonate sensor.	Bicarbonates	278-289	microRNA 506	Homo sapiens	47-54
28849090-12	2017	The overexpression of miR-506 and miR-214 reversed the H2O2-induced apoptosis and increase of ROS in the HCMs.	Reactive Oxygen Species	94-97	microRNA 506	Homo sapiens	22-29
28849090-13	2017	In conclusion, the overexpression of miR-506 and miR-214 were confirmed to have a protective effect against H2O2-induced HCM injury by suppressing the expression of KLF4 and KLF5.	Hydrogen Peroxide	108-112	microRNA 506	Homo sapiens	37-44
28849090-11	2017	The overexpression of miR-506 and miR-124 inhibited the H2O2-induced upregulation of KLF4 and KLF5 in the HCMs.	Hydrogen Peroxide	56-60	microRNA 506	Homo sapiens	22-29
28849090-12	2017	The overexpression of miR-506 and miR-214 reversed the H2O2-induced apoptosis and increase of ROS in the HCMs.	Hydrogen Peroxide	55-59	microRNA 506	Homo sapiens	22-29
28217977-0	2017	miR-506 enhances the sensitivity of human colorectal cancer cells to oxaliplatin by suppressing MDR1/P-gp expression.	Oxaliplatin	69-80	microRNA 506	Homo sapiens	0-7
28217977-2	2017	The aim of this study was to elucidate the mechanism by which miR-506 reverses oxaliplatin chemoresistance in CRC.	Oxaliplatin	79-90	microRNA 506	Homo sapiens	62-69
28217977-12	2017	miR-506 overexpression inhibited cell growth and increased oxaliplatin-induced cell apoptosis in HCT116-OxR cells, as shown via FCM and apoptosis assay.	Oxaliplatin	59-70	microRNA 506	Homo sapiens	0-7
28217977-15	2017	CONCLUSION: Taken together, the findings of our study demonstrate that miR-506 overexpression in HCT116-OxR cells enhances oxaliplatin sensitivity by inhibiting MDR1/P-gp expression via down-regulation of the Wnt/beta-catenin pathway and thus provide a rationale for the development of miRNA-based strategies to reverse oxaliplatin resistance in CRC cells.	Oxaliplatin	123-134	microRNA 506	Homo sapiens	71-78
28217977-15	2017	CONCLUSION: Taken together, the findings of our study demonstrate that miR-506 overexpression in HCT116-OxR cells enhances oxaliplatin sensitivity by inhibiting MDR1/P-gp expression via down-regulation of the Wnt/beta-catenin pathway and thus provide a rationale for the development of miRNA-based strategies to reverse oxaliplatin resistance in CRC cells.	Oxaliplatin	320-331	microRNA 506	Homo sapiens	71-78
27371108-8	2016	Moreover, miR-506 expression was negatively associated with pathologic T category (P = 0.004) and lymph node metastasis (P = 0.033), suggesting that miR-506 might inhibit the progression of PDAC.	pdac	190-194	microRNA 506	Homo sapiens	10-17
28121485-10	2017	These findings expand the known mechanisms of MIR506-mediated tumor suppression to activation of autophagy-related cell death and suggest a strategy for using MIR506 as an anti-STAT3 approach to PDAC treatment.	pdac	195-199	microRNA 506	Homo sapiens	46-52
28121485-10	2017	These findings expand the known mechanisms of MIR506-mediated tumor suppression to activation of autophagy-related cell death and suggest a strategy for using MIR506 as an anti-STAT3 approach to PDAC treatment.	pdac	195-199	microRNA 506	Homo sapiens	159-165
27371108-8	2016	Moreover, miR-506 expression was negatively associated with pathologic T category (P = 0.004) and lymph node metastasis (P = 0.033), suggesting that miR-506 might inhibit the progression of PDAC.	pdac	190-194	microRNA 506	Homo sapiens	149-156
27371108-9	2016	CONCLUSIONS: Our results suggest that miR-506 either plays a role as an oncogene in the tumorigenesis and a tumor suppressor in the progression or serves as a house-keeping, tumor-suppressing miRNA, whose expression can be activated by oncogenic signals in early development to hinder the progression of PDAC.	pdac	304-308	microRNA 506	Homo sapiens	38-45
26398880-4	2015	Subsequently, gain-of-function and loss-of-function experiments were performed in vitro, and the results from MTT assay, Transwell-Matrigel invasion assay and cell adhesion assay revealed that miR-506 suppresses cell proliferation, invasion and adhesion of breast cancer cells.	monooxyethylene trimethylolpropane tristearate	110-113	microRNA 506	Homo sapiens	193-200
27114802-0	2016	miR-506 inhibits cell proliferation and invasion by targeting TET family in colorectal cancer.	tet	62-65	microRNA 506	Homo sapiens	0-7
27114802-8	2016	We showed that TET family member degradation by miR-506 inhibits cell proliferation and invasion in colorectal cancer.	tet	15-18	microRNA 506	Homo sapiens	48-55
27114802-9	2016	CONCLUSION: Through this study, we advance our understanding of the expression levels TETs and miR-506 in CRC and further clarify the internal regulatory mechanism of miR-506 by targeting TET during CRC processes.	tetramethylenedisulfotetramine	86-90	microRNA 506	Homo sapiens	167-174
27114802-9	2016	CONCLUSION: Through this study, we advance our understanding of the expression levels TETs and miR-506 in CRC and further clarify the internal regulatory mechanism of miR-506 by targeting TET during CRC processes.	tet	86-89	microRNA 506	Homo sapiens	167-174
24469051-2	2015	Here we report that miR-506 upregulation occurs in 83% of lung cancer patients (156 cases), and its expression highly correlates with ROS.	Reactive Oxygen Species	134-137	microRNA 506	Homo sapiens	20-27
26369335-4	2015	Further functional study demonstrated that miR-506 could augment the response to cisplatin and olaparib through targeting RAD51 and suppressing homologous recombination in a panel of ovarian cancer cell lines.	Cisplatin	81-90	microRNA 506	Homo sapiens	43-50
26369335-4	2015	Further functional study demonstrated that miR-506 could augment the response to cisplatin and olaparib through targeting RAD51 and suppressing homologous recombination in a panel of ovarian cancer cell lines.	olaparib	95-103	microRNA 506	Homo sapiens	43-50
26369335-5	2015	Systemic delivery of miR-506 in an orthotopic ovarian cancer mouse model significantly augmented the cisplatin response, thus recapitulating the clinical observation.	Cisplatin	101-110	microRNA 506	Homo sapiens	21-28
24469051-3	2015	Ectopic expression of miR-506 inhibits NF-kappaB p65 expression, induces ROS accumulation and then activates p53 to suppress lung cancer cell viability, but not in normal cells.	Reactive Oxygen Species	73-76	microRNA 506	Homo sapiens	22-29
24469051-4	2015	Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS.	Reactive Oxygen Species	129-132	microRNA 506	Homo sapiens	28-35
24469051-4	2015	Interestingly, p53 promotes miR-506 expression level, indicating that miR-506 mediates cross talk between p53, NF-kappaB p65 and ROS.	Reactive Oxygen Species	129-132	microRNA 506	Homo sapiens	70-77
21726609-0	2011	The role of miR-506 in transformed 16HBE cells induced by anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide.	16hbe	35-40	microRNA 506	Homo sapiens	12-19
25378392-10	2015	Histamine-induced, InsP3-mediated Ca(2+) signals were decreased by 50% in stable miR-506 cells compared with controls.	Histamine	0-9	microRNA 506	Homo sapiens	81-88
21726609-0	2011	The role of miR-506 in transformed 16HBE cells induced by anti-benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide.	benzo[a]pyrene-trans-7,8-dihydrodiol-9,10-epoxide	63-112	microRNA 506	Homo sapiens	12-19