PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
29115452-10	2018	Restoration of calpain-2 in miR-93-overexpresseing SUI primary fibroblasts reversed the alteration in hydroxyproline expression, indicating that calpain-2 was negatively associated with collagen expression.	Hydroxyproline	102-116	microRNA 9-3	Homo sapiens	28-34
29434867-8	2018	Re-expression of miR-93 promoted cell growth in vitro as determined by the MTT assay.	monooxyethylene trimethylolpropane tristearate	75-78	microRNA 9-3	Homo sapiens	17-23
29109127-4	2018	The regulatory locus also expresses two functional RNAs, LINC00925-RNA and MIR9-3, which are coexpressed with POLG The MIR9-3 targets include NR2E1, a transcription factor maintaining neural stem cells in undifferentiated state, and MTHFD2, the regulatory enzyme of mitochondrial folate cycle, linking POLG expression to stem cell differentiation and folate metabolism.	Folic Acid	280-286	microRNA 9-3	Homo sapiens	119-125
29109127-4	2018	The regulatory locus also expresses two functional RNAs, LINC00925-RNA and MIR9-3, which are coexpressed with POLG The MIR9-3 targets include NR2E1, a transcription factor maintaining neural stem cells in undifferentiated state, and MTHFD2, the regulatory enzyme of mitochondrial folate cycle, linking POLG expression to stem cell differentiation and folate metabolism.	Folic Acid	351-357	microRNA 9-3	Homo sapiens	119-125
29116087-10	2017	Free testosterone and free androgen index were positively correlated with expression of miR-93 and miR-21 in GCs of PCOS group.	Testosterone	5-17	microRNA 9-3	Homo sapiens	88-94
29243790-1	2017	OBJECTIVE: To identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis.	oxygen-glucose	73-87	microRNA 9-3	Homo sapiens	49-60
29243790-1	2017	OBJECTIVE: To identify the expression changes of microRNA 93 (miR-93) in oxygen-glucose deprivation/reoxygenation (OGD/R) injury in cardiomyocytes and its mechanism of mediating OGD/R and inducing apoptosis.	oxygen-glucose	73-87	microRNA 9-3	Homo sapiens	62-68
28765915-4	2017	Overexpressed miR-93 in sensitive cells revealed increases in cellular proliferation and the expression levels of drug-resistant-related genes, and a decrease in sensitivity to doxorubicin.	Doxorubicin	177-188	microRNA 9-3	Homo sapiens	14-20
28260112-5	2017	In the present study, we showed that miR-9-3p (miR-9) was downregulated in adriamycin (ADR)-resistant K562/ADR cells and CML/MDR patients.	Doxorubicin	75-85	microRNA 9-3	Homo sapiens	37-45
28804566-1	2017	We investigated the ability of microRNA-93 (miR-93) to influence proliferation, invasion, migration, and apoptosisofrenal cell carcinoma (RCC) cells via transforming growth factor-beta/solvated metal atom dispersed (TGF-beta/Smad) signaling by targeting runt-related transcription factor 3 (RUNX3).	Metals	194-199	microRNA 9-3	Homo sapiens	31-42
28804566-1	2017	We investigated the ability of microRNA-93 (miR-93) to influence proliferation, invasion, migration, and apoptosisofrenal cell carcinoma (RCC) cells via transforming growth factor-beta/solvated metal atom dispersed (TGF-beta/Smad) signaling by targeting runt-related transcription factor 3 (RUNX3).	Metals	194-199	microRNA 9-3	Homo sapiens	44-50
28613134-4	2017	By transfection of miR-9-3p mimics in CNE-1, CNE-2 and HONE-1 cells, we confirmed tumor-suppressing roles of miR-9-3p via suppressing EMT process by MTT, wound scratch, transwell assay and western blot.	monooxyethylene trimethylolpropane tristearate	149-152	microRNA 9-3	Homo sapiens	109-117
28430789-0	2017	MiR-9-3p augments apoptosis induced by H2O2 through down regulation of Herpud1 in glioma.	Hydrogen Peroxide	39-43	microRNA 9-3	Homo sapiens	0-7
28430789-7	2017	Glioma cells transfected with miR-9-3p mimics or HERPUD1-RNAi had more apoptotic cells than them in control after induced by H2O2.	Hydrogen Peroxide	125-129	microRNA 9-3	Homo sapiens	30-38
28384720-5	2017	Results: The frequency of low copy numbers of miR-143, miR-146a, miR-9-3, and miR-205 and of high copy numbers of miR-301a and miR-23a was increased in patients with AAU+AS+ (P = 3.725 x 10-5 to 8.033 x 10-9).	aau	166-169	microRNA 9-3	Homo sapiens	65-72
28384720-10	2017	Conclusions: Low gene copy numbers of miR-143, miR-146a, miR-9-3, miR-205 and high gene copy numbers of miR-301a and miR-23a were associated with susceptibility to AAU+AS+.	aau	164-167	microRNA 9-3	Homo sapiens	57-64
28056303-3	2016	MiR-93 down-regulated 143B and HuO9 cells were constructed by lipofection transfection, and their proliferation and apoptosis were detected by MTT and flow cytometry assays, respectively.	monooxyethylene trimethylolpropane tristearate	143-146	microRNA 9-3	Homo sapiens	0-6
28056303-7	2016	MTT and flow cytometry assays showed that miR-93 promoted proliferation and inhibited apoptosis in osteosarcoma cells.	monooxyethylene trimethylolpropane tristearate	0-3	microRNA 9-3	Homo sapiens	42-48
26459099-6	2015	To investigate this, an MTT assay was used to determine cell proliferation, and the effects of miRNA-9-3p on triglycerides (TG) and total cholesterol (TC) in the HepG2 cells were also examined.	Triglycerides	109-122	microRNA 9-3	Homo sapiens	95-105
27119510-6	2016	Furthermore, miR-93 mimic significantly increased p-Akt levels under H/R, which was partially released by LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	106-114	microRNA 9-3	Homo sapiens	13-19
27099514-4	2016	Higher levels of miR-93 were observed in the cisplatin-resistant BC cell line RT4, compared to the cell line T24.	Cisplatin	45-54	microRNA 9-3	Homo sapiens	17-23
27099514-6	2016	We found that inhibiting miR-93 promoted cisplatin-induced apoptosis due to the accumulation of DNA damage.	Cisplatin	41-50	microRNA 9-3	Homo sapiens	25-31
27878244-11	2016	Therefore, miR-93 was capable of inhibiting viability and inducing apoptosis of the GTM cells, which was achieved via the suppression of NFE2L2.	O1-METHYL-4-DEOXY-4-THIO-BETA-D-GLUCOSE	84-87	microRNA 9-3	Homo sapiens	11-17
27185265-0	2016	MicroRNA-93 promotes the malignant phenotypes of human glioma cells and induces their chemoresistance to temozolomide.	Temozolomide	105-117	microRNA 9-3	Homo sapiens	0-11
27185265-9	2016	In addition, inhibition of miR-93 enhanced the chemosensitization of glioma cells to temozolomide (TMZ).	Temozolomide	85-97	microRNA 9-3	Homo sapiens	27-33
27185265-9	2016	In addition, inhibition of miR-93 enhanced the chemosensitization of glioma cells to temozolomide (TMZ).	Temozolomide	99-102	microRNA 9-3	Homo sapiens	27-33
27185265-10	2016	Based on these above data, our study demonstrates that miR-93, upregulated in glioma, promotes the proliferation, cell cycle progression, migration and invasion of human glioma cells and suppresses their chemosensitivity to TMZ.	Temozolomide	224-227	microRNA 9-3	Homo sapiens	55-61
29798051-1	2016	Objective:To investigate the expression of has-miR-93-5p on human laryngeal squamous cell carcinoma and the influence on malignant phenotype of Hep-2 cell.Method:The expression of has-miR-93-5p of paraffin samples in LSCC was determined by looped-primer Real-time PCR, and the relationship between the expression and the clinical pathological parameters was analysed.	Paraffin	197-205	microRNA 9-3	Homo sapiens	184-190
26582398-10	2015	In conclusion, circulating miRNA-93 and miRNA-223 were higher in women with PCOS compared to age and weight matched controls independent of insulin resistance and testosterone levels, and miR-93 may represent a novel diagnostic biomarker for PCOS.	Testosterone	163-175	microRNA 9-3	Homo sapiens	27-35
26459099-8	2015	The date revealed that downregulation of miRNA-9-3p inhibited the proliferation of HepG2 cells, and significantly reduced the accumulation of lipids, and decreased TG and TC content.	Technetium	171-173	microRNA 9-3	Homo sapiens	41-51
25831546-6	2015	Enforced expression of miR-93 in ovarian CSCs reduced Pol eta expression and increased their sensitivity to cisplatin.	Cisplatin	108-117	microRNA 9-3	Homo sapiens	23-29
25892549-5	2015	The MTT assay, colony formation assay, anchorage-independent growth, and Transwell migration and invasion assays showed that depletion of miR-93 inhibited NPC cell growth, invasion and migration in vitro and suppressed tumor growth in vivo.	monooxyethylene trimethylolpropane tristearate	4-7	microRNA 9-3	Homo sapiens	138-144
25831546-8	2015	Targeting Pol eta, probably through enhancement of miR-93 expression, might be exploited as a strategy to increase the efficacy of cisplatin treatment.	Cisplatin	131-140	microRNA 9-3	Homo sapiens	51-57
25785043-8	2015	Meanwhile, our results indicate that the serum miR-93 positively correlates with the serum cholesterol level.	Cholesterol	91-102	microRNA 9-3	Homo sapiens	47-53
25371073-8	2015	These findings showed that miR-93 suppresses colorectal cancer development via downregulating Wnt/beta-catenin, at least in part, by targeting Smad7.	wnt	94-97	microRNA 9-3	Homo sapiens	27-33
25633810-8	2015	miR-93 also rendered cells to be more sensitive to sorafenib and tivantinib treatment.	Sorafenib	51-60	microRNA 9-3	Homo sapiens	0-6
25633810-8	2015	miR-93 also rendered cells to be more sensitive to sorafenib and tivantinib treatment.	ARQ 197	65-75	microRNA 9-3	Homo sapiens	0-6
25393367-5	2015	RESULTS: SAHA upregulates the transcription of MICA/B by promoting MICA-associated histone acetylation while suppressing the MICA/B-targeting miRNAs miR-20a, miR-93 and miR-106b.	Vorinostat	9-13	microRNA 9-3	Homo sapiens	158-164
26087719-0	2015	Berberine Sensitizes Human Ovarian Cancer Cells to Cisplatin Through miR-93/PTEN/Akt Signaling Pathway.	Berberine	0-9	microRNA 9-3	Homo sapiens	69-75
26273679-3	2015	Overexpressed miR-93 directly inhibited glucose transporter isoform 4 (GLUT4) expression, thereby influencing glucose metabolism.	Glucose	40-47	microRNA 9-3	Homo sapiens	14-20
26087719-0	2015	Berberine Sensitizes Human Ovarian Cancer Cells to Cisplatin Through miR-93/PTEN/Akt Signaling Pathway.	Cisplatin	51-60	microRNA 9-3	Homo sapiens	69-75
26087719-8	2015	Next, we observed that the miR-93 levels in cisplatin resistant cell lines were higher than that in cisplatin sensitive cell lines.	Cisplatin	44-53	microRNA 9-3	Homo sapiens	27-33
26087719-8	2015	Next, we observed that the miR-93 levels in cisplatin resistant cell lines were higher than that in cisplatin sensitive cell lines.	Cisplatin	100-109	microRNA 9-3	Homo sapiens	27-33
26087719-9	2015	Furthermore, our study found berberine could inhibit miR-93 expression and function in ovarian cancer, as shown by an increase of its target PTEN, an important tumor suppressor in ovarian cancer.	Berberine	29-38	microRNA 9-3	Homo sapiens	53-59
26087719-12	2015	CONCLUSION: The results suggested that berberine modulated the sensitivity of cisplatin through miR-93/PTEN/AKT signaling pathway in the ovarian cancer cells.	Berberine	39-48	microRNA 9-3	Homo sapiens	96-102
26087719-12	2015	CONCLUSION: The results suggested that berberine modulated the sensitivity of cisplatin through miR-93/PTEN/AKT signaling pathway in the ovarian cancer cells.	Cisplatin	78-87	microRNA 9-3	Homo sapiens	96-102
25094038-5	2014	After validation by real-time PCR, all three members of the miR-106b-25 cluster (miR-106b, miR-93, and miR-25) were found to be markedly down-regulated during EMT in response to TGF-beta1, whereas these miRNAs were up-regulated by Sal B treatment in a dose-dependent manner.	salvianolic acid B	231-236	microRNA 9-3	Homo sapiens	91-97
23493574-8	2013	These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome.	Glucose	75-82	microRNA 9-3	Homo sapiens	94-100
24606013-0	2014	Expression level of miR-93 in formalin-fixed paraffin-embedded tissues of breast cancer patients.	Formaldehyde	30-38	microRNA 9-3	Homo sapiens	20-26
24606013-0	2014	Expression level of miR-93 in formalin-fixed paraffin-embedded tissues of breast cancer patients.	Paraffin	45-53	microRNA 9-3	Homo sapiens	20-26
24606013-2	2014	The objective of this study was to evaluate the potential predictive value of miR-93 expression in formalin-fixed paraffin-embedded (FFPE) tissues of breast cancer patients.	Formaldehyde	99-107	microRNA 9-3	Homo sapiens	78-84
24606013-2	2014	The objective of this study was to evaluate the potential predictive value of miR-93 expression in formalin-fixed paraffin-embedded (FFPE) tissues of breast cancer patients.	Paraffin	114-122	microRNA 9-3	Homo sapiens	78-84
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	45-52
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	101-108
24373626-7	2013	5-Aza-2"-deoxycytidine treatment resulted in miR-9-3 promoter demethylation and re-expression of pri-miR-9-3 in I83-E95 and WAC3CD5+ cells, which were homozygously methylated for miR-9-3.	Decitabine	0-22	microRNA 9-3	Homo sapiens	101-108
23530058-4	2013	Screening of a miRNA mimic library revealed the ability of miR-9-3p to significantly enhance AZD6244-induced extracellular signal-regulated kinase inhibition and growth arrest, while miR-9-3p had little effect on growth alone.	AZD 6244	93-100	microRNA 9-3	Homo sapiens	59-67
23530058-7	2013	The beta1 integrin gene (ITGB1) was identified as a new miR-9-3p target, and the growth inhibition seen with small interfering RNA knockdown or antibody blocking of ITGB1 in combination with MEK inhibitor phenocopied the growth inhibition seen with miR-9-3p plus AZD6244.	AZD 6244	263-270	microRNA 9-3	Homo sapiens	56-64
23611780-8	2013	Snail protein expression was higher in CL than that in EV cells and H1299 cells exhibited an increase in the expression of Snail upon transient transfection with miR-93.	.alpha.-Glutamylvaline	55-57	microRNA 9-3	Homo sapiens	162-168
23192662-7	2013	Treatment of both cell lines with either 50 muM EGC or 50 muM EGCG decreased expression of the OGmiRs (miR-92, miR-93, and miR-106b) and increased expression of the TSmiRs (miR-7-1, miR-34a, and miR-99a) leading to induction of extrinsic and intrinsic pathways of apoptosis.	gallocatechol	48-51	microRNA 9-3	Homo sapiens	111-117
23492819-7	2013	We demonstrate an increased expression of the miR-93 in E2-treated mammary tissues and in human breast cell lines and vit C treatment reverted E2-mediated increase in miR-93 levels.	Ascorbic Acid	118-123	microRNA 9-3	Homo sapiens	46-52
23492819-7	2013	We demonstrate an increased expression of the miR-93 in E2-treated mammary tissues and in human breast cell lines and vit C treatment reverted E2-mediated increase in miR-93 levels.	Ascorbic Acid	118-123	microRNA 9-3	Homo sapiens	167-173
23192662-7	2013	Treatment of both cell lines with either 50 muM EGC or 50 muM EGCG decreased expression of the OGmiRs (miR-92, miR-93, and miR-106b) and increased expression of the TSmiRs (miR-7-1, miR-34a, and miR-99a) leading to induction of extrinsic and intrinsic pathways of apoptosis.	epigallocatechin gallate	62-66	microRNA 9-3	Homo sapiens	111-117
22465665-0	2012	Involvement of microRNA-93, a new regulator of PTEN/Akt signaling pathway, in regulation of chemotherapeutic drug cisplatin chemosensitivity in ovarian cancer cells.	Cisplatin	114-123	microRNA 9-3	Homo sapiens	15-26
24356455-8	2013	Treatment with 5-AzaC concomitantly upregulated expression of miR-9-3 and miR-193a, and downregulated their respective target genes NF-kappaB and Mcl-1.	Decitabine	15-21	microRNA 9-3	Homo sapiens	62-69
24356455-11	2013	CONCLUSIONS: Methylation-silencing of miR-9-3 and miR-193a may be an important epigenetic mechanisms favoring NSCLC cell growth and survival for carcinogenesis and cancer progression, and demethylation to reactivate expression of miR-9-3 and miR-193a genes contributes, at least partially, to the anti-cancer properties of 5-AzaC and thereby may be worthy of future studies for the possibility of being a new therapeutic strategy for the treatment of human NSCLCs.	Decitabine	323-329	microRNA 9-3	Homo sapiens	38-45
22498172-3	2012	Combination of 4-HPR and EGCG most significantly decreased expression of OGmiRs (miR-92, miR-93, and miR-106b) and increased expression of TSmiRs (miR-7-1, miR-34a, and miR-99a) in both cell lines.	epigallocatechin gallate	25-29	microRNA 9-3	Homo sapiens	89-95
22556343-4	2012	Assessing the regulatory function of miR-93/106b through doxycycline-inducible lentiviral transduction in a microarray analysis, tissue factor (F3) and IL8 were identified as their possible targets.	Doxycycline	57-68	microRNA 9-3	Homo sapiens	37-43
22465665-3	2012	In this paper, we utilized microRNA array and real-time PCR to show that miR-93 is significantly up-regulated in cisplatin-resistant ovarian cancer cells.	Cisplatin	113-122	microRNA 9-3	Homo sapiens	73-79
22465665-4	2012	In vitro assays show that over-expression and knock-down of miR-93 regulate apoptotic activity, and thereby cisplatin chemosensitivity, in ovarian cells.	Cisplatin	108-117	microRNA 9-3	Homo sapiens	60-66
22465665-6	2012	MiR-93 inversely correlates with PTEN expression in CDDP-resistant and sensitive human ovarian cancer tissues.	Cisplatin	52-56	microRNA 9-3	Homo sapiens	0-6
21235780-8	2011	CONCLUSIONS: Our results confirm that 454 sequencing of bisulfite treated genomic DNA provides reliable high quality quantitative methylation data and identify MAL, hsa-mir-9-3, hsa-mir-596, and hsa-mir-663 as new targets of aberrant DNA methylation in human hepatocellular carcinoma.	hydrogen sulfite	56-65	microRNA 9-3	Homo sapiens	165-176
21831295-12	2011	CONCLUSIONS: Together, our findings demonstrate that miR-93 and miR-155 constitutively suppress AID translation in MCF-7 cells, suggesting widespread roles for these miRs in preventing genome cytidine deaminations, mutagenesis, and oncogenic transformation.	Cytidine	192-200	microRNA 9-3	Homo sapiens	53-59
34187448-11	2021	HCP5 knockdown or miR-93-5p restoration ameliorated HG-induced HGMC proliferation, fibrosis and inflammation.	Mercury	52-54	microRNA 9-3	Homo sapiens	18-24
19549897-5	2009	Repressive chromatin marks, trimethyl Lys27 of histone H3 (H3K27me3) and dimethyl Lys9 of histone H3 (H3K9me2), were found at a down-regulated locus, miR-9-3, in epithelial cells preexposed to diethylstilbestrol.	trimethyl lys27	28-43	microRNA 9-3	Homo sapiens	150-157
19549897-5	2009	Repressive chromatin marks, trimethyl Lys27 of histone H3 (H3K27me3) and dimethyl Lys9 of histone H3 (H3K9me2), were found at a down-regulated locus, miR-9-3, in epithelial cells preexposed to diethylstilbestrol.	Diethylstilbestrol	193-211	microRNA 9-3	Homo sapiens	150-157
34435526-13	2021	miR-93-5p targeted TETs to modulate ERBB4 abundance.	tetramethylenedisulfotetramine	19-23	microRNA 9-3	Homo sapiens	0-6
34552061-0	2021	MiR-9-3p regulates the biological functions and drug resistance of gemcitabine-treated breast cancer cells and affects tumor growth through targeting MTDH.	gemcitabine	67-78	microRNA 9-3	Homo sapiens	0-8
34552061-7	2021	Moreover, miR-9-3p had a targeted binding relationship with MTDH, and overexpressed miR-9-3p greatly promoted the toxic effects of Gem on cancer cells and expressions of apoptosis-related proteins, whereas overexpressed MTDH partially reversed such effects of overexpressed miR-9-3p.	gemcitabine	131-134	microRNA 9-3	Homo sapiens	10-18
34552061-7	2021	Moreover, miR-9-3p had a targeted binding relationship with MTDH, and overexpressed miR-9-3p greatly promoted the toxic effects of Gem on cancer cells and expressions of apoptosis-related proteins, whereas overexpressed MTDH partially reversed such effects of overexpressed miR-9-3p.	gemcitabine	131-134	microRNA 9-3	Homo sapiens	84-92
34552061-8	2021	The study proved that miR-9-3p regulates biological functions, drug resistance, and the growth of Gem-treated breast cancer cells through targeting MTDH.	gemcitabine	98-101	microRNA 9-3	Homo sapiens	22-30
35377979-7	2022	These investigations demonstrated that promoting effect of miR-93-5p on HCC cell growth may be carried out by inhibiting the PCK1 expression, suggesting that miR-93-5p and PCK1 could be applied as new biomarkers or novel therapeutic targets for HCC diagnosis.	-93-5p	161-167	microRNA 9-3	Homo sapiens	59-65
34162560-1	2021	OBJECTIVE: To investigate the role and potential underlying mechanism of miR-93-5p in the carcinogenesis and gemcitabine resistance of pancreatic cancer (PC) cells.	gemcitabine	109-120	microRNA 9-3	Homo sapiens	73-79
34162560-12	2021	CONCLUSION: These observations suggest that miR-93-5p modulates tumorigenesis and gemcitabine resistance in PC cells via targeting the PTEN/PI3K/Akt signaling pathway.	gemcitabine	82-93	microRNA 9-3	Homo sapiens	44-50
35625825-9	2022	We also analyzed the expression of several microRNAs and found that melatonin enhanced the effect of radiation on the levels of miR-20a, miR-19a, miR-93, miR-20b and miR-29a.	Melatonin	68-77	microRNA 9-3	Homo sapiens	146-152
34035852-11	2021	However, miR-9-3p inhibitor and IGF1R overexpression reversed DUXAP8 knockdown- and miR-9-3p overexpression-induced effects, respectively.	duxap8	62-68	microRNA 9-3	Homo sapiens	9-17
33831356-5	2021	In addition, miR-93 was found highly expressed in cisplatin or sorafenib-resistant liver cancer tissues.	Cisplatin	50-59	microRNA 9-3	Homo sapiens	13-19
33831356-5	2021	In addition, miR-93 was found highly expressed in cisplatin or sorafenib-resistant liver cancer tissues.	Sorafenib	63-72	microRNA 9-3	Homo sapiens	13-19
33831356-6	2021	Interference of miR-93 sensitizes hepatoma cells to cisplatin or sorafenib treatment.	Cisplatin	52-61	microRNA 9-3	Homo sapiens	16-22
33831356-6	2021	Interference of miR-93 sensitizes hepatoma cells to cisplatin or sorafenib treatment.	Sorafenib	65-74	microRNA 9-3	Homo sapiens	16-22
33831356-7	2021	Clinical cohort analysis showed that Hepatocellular carcinoma (HCC) patients with low miR-93 were benefit more from TACE or sorafenib treatment.	Sorafenib	124-133	microRNA 9-3	Homo sapiens	86-92
33760164-13	2021	Following co-transfection with HGF overexpression vector and miR-93-5p mimic, miR-93-5p mimic-mediated induction of HepG2 cell proliferation, glucose consumption and glycogen synthesis in insulin-resistant HepG2 cells was inhibited.	Glycogen	166-174	microRNA 9-3	Homo sapiens	61-67
33760164-13	2021	Following co-transfection with HGF overexpression vector and miR-93-5p mimic, miR-93-5p mimic-mediated induction of HepG2 cell proliferation, glucose consumption and glycogen synthesis in insulin-resistant HepG2 cells was inhibited.	Glycogen	166-174	microRNA 9-3	Homo sapiens	78-84
33959659-13	2021	Conclusions: miR-93-5p expression was associated with the severity of CTEPH and could act as a potential predictor of high-risk CTEPH.	cteph	70-75	microRNA 9-3	Homo sapiens	13-19
33959659-13	2021	Conclusions: miR-93-5p expression was associated with the severity of CTEPH and could act as a potential predictor of high-risk CTEPH.	cteph	128-133	microRNA 9-3	Homo sapiens	13-19
32426273-8	2020	Then, the anti-cancer drug 5-fluorouracil was used to stimulate the NCI-H460 cells; the mRNA levels of miR-93, miR-373, and miR-17-5p were decreased, and the level of TBP-2 mRNA and protein was increased.	Fluorouracil	27-41	microRNA 9-3	Homo sapiens	103-109
32335549-7	2021	Notably, treatment with the histone deacetylase inhibitor Vorinostat (SAHA) reduces miR-93 expression and enhances p21 expression in the malignant T cells.	Vorinostat	58-68	microRNA 9-3	Homo sapiens	84-90
33463130-0	2020	Epigallocatechin-3-gallate Enhances the Efficacy of MicroRNA-34a Mimic and MicroRNA-93 Inhibitor Co-transfection in Prostate Cancer Cell Line.	epigallocatechin gallate	0-26	microRNA 9-3	Homo sapiens	75-86
32086547-8	2020	Five microRNAs (miR-20a, miR-92a, miR-93, miR-195, miR-451) had a highly significant correlation with normalized urinary albumin, serum creatinine at 24 h and creatinine clearance.	Creatinine	136-146	microRNA 9-3	Homo sapiens	34-40
32086547-8	2020	Five microRNAs (miR-20a, miR-92a, miR-93, miR-195, miR-451) had a highly significant correlation with normalized urinary albumin, serum creatinine at 24 h and creatinine clearance.	Creatinine	159-169	microRNA 9-3	Homo sapiens	34-40
32086547-12	2020	A set of microRNAs (miR-20a, miR-92a, miR-93, miR-195, miR-451) could be promising biomarkers for early detection of oxalic acid-induced acute kidney injury.	Oxalic Acid	117-128	microRNA 9-3	Homo sapiens	38-44
32473920-6	2020	The effect of MEG3 and miR-93 on high glucose (HG)-induced apoptosis was detected by MTT and flow cytometry.	Glucose	38-45	microRNA 9-3	Homo sapiens	23-29
32473920-6	2020	The effect of MEG3 and miR-93 on high glucose (HG)-induced apoptosis was detected by MTT and flow cytometry.	Mercury	47-49	microRNA 9-3	Homo sapiens	23-29
32473920-6	2020	The effect of MEG3 and miR-93 on high glucose (HG)-induced apoptosis was detected by MTT and flow cytometry.	monooxyethylene trimethylolpropane tristearate	85-88	microRNA 9-3	Homo sapiens	23-29
31836624-9	2020	Transfection of K562 cells with miR-9-3p or miR-9-5p mimics led to decreased TOP2alpha/170 protein levels without a change in TOP2alpha/170 mRNA, and resulted in attenuated etoposide-induced DNA damage (gain-of-miRNA-inhibitory function).	Etoposide	173-182	microRNA 9-3	Homo sapiens	32-40
31836624-10	2020	Conversely, transfection of miR-9-3p or miR-9-5p inhibitors in K/VP.5 cells (overexpressed miR-9 and low TOP2alpha/170) led to increased TOP2alpha/170 protein expression without a change in TOP2alpha/170 mRNA, and resulted in enhancement of etoposide-induced DNA damage (loss-of-miRNA-inhibitory function).	Etoposide	241-250	microRNA 9-3	Homo sapiens	28-36
31836624-12	2020	SIGNIFICANCE STATEMENT: Results presented here indicate that miR-9-3p and miR-9-5p decrease TOP2alpha/170 expression levels in acquired resistance to etoposide.	Etoposide	150-159	microRNA 9-3	Homo sapiens	61-69
31432162-0	2019	Cisplatin decreases cyclin D2 expression via upregulating miR-93 to inhibit lung adenocarcinoma cell growth.	Cisplatin	0-9	microRNA 9-3	Homo sapiens	58-64
31937854-6	2020	The plasma levels of four miRs; miR-93-5p, -141-3p, -221-3p, and miR-375-3p decreased significantly after treatment initiation in patients receiving docetaxel, and for miR-141-3p and miR-375-3p the level increased again at the time of radiological progression.	docetaxel	149-158	microRNA 9-3	Homo sapiens	32-38
32046397-4	2020	However, it remains unknown whether miR-93 is associated with human RSA.	rabbit sperm membrane autoantigen	68-71	microRNA 9-3	Homo sapiens	36-42
32046397-10	2020	Collectively, these data strongly suggest that miR-93 regulates trophoblast cell proliferation, migration, invasive, and apoptosis by targeting BCL2L2 expression and is involved in the pathogenesis of RSA.	rabbit sperm membrane autoantigen	201-204	microRNA 9-3	Homo sapiens	47-53
31432162-4	2019	Cisplatin induced cell apoptosis and inhibited cell migration by increasing the levels of miR-93, miR-26a and miR-26b.	Cisplatin	0-9	microRNA 9-3	Homo sapiens	90-96
31432162-7	2019	In vivo analysis further supported that cisplatin inhibited lung adenocarcinoma cell growth by regulating cyclin D2 and miR-93 expression.	Cisplatin	40-49	microRNA 9-3	Homo sapiens	120-126
31432162-8	2019	In conclusion, our findings demonstrated that cisplatin could effectively inhibit lung adenocarcinoma cell proliferation by decreasing cyclin D2 expression via miR-93.	Cisplatin	46-55	microRNA 9-3	Homo sapiens	160-166
30903189-0	2019	Circular RNA 0039411 Is Involved in Neodymium Oxide-induced Inflammation and Antiproliferation in a Human Bronchial Epithelial Cell Line via Sponging miR-93-5p.	neodymium oxide	36-51	microRNA 9-3	Homo sapiens	150-156
31301086-7	2019	Mechanistically, we found that circCRIM1 could promote the expression of leukemia inhibitory factor receptor, a well-known tumor suppressor, by sponging miR-93 and miR-182.	circcrim1	31-40	microRNA 9-3	Homo sapiens	153-159
30903189-11	2019	These results suggested that upregulation of circ_0039411 mediated Nd2O3-induced inflammation and dysfunction by sponging miR-93-5p.	neodymium oxide	67-72	microRNA 9-3	Homo sapiens	122-128
30654687-5	2019	Moreover, two first-line treatments for GBM, IR and temozolomide (TMZ), as well as rapamycin (Rap), the prototypic MTOR inhibitor, decreased MIR93 expression that, in turn, stimulated autophagic processes in GSCs.	Temozolomide	52-64	microRNA 9-3	Homo sapiens	141-146
30654687-5	2019	Moreover, two first-line treatments for GBM, IR and temozolomide (TMZ), as well as rapamycin (Rap), the prototypic MTOR inhibitor, decreased MIR93 expression that, in turn, stimulated autophagic processes in GSCs.	Temozolomide	66-69	microRNA 9-3	Homo sapiens	141-146
30342140-7	2019	As expected, GTP (25, 50 and 100 mug/ml) inhibited growth of PC-3 cells via inducing apoptosis, which was achieved by elevation of bax/bcl-2 ratio and caspae-3 protein expression, as well as a decrease of miR-93.	Guanosine Triphosphate	13-16	microRNA 9-3	Homo sapiens	205-211
31128026-0	2019	L-Tetrahydropalmatine enhances the sensitivity of human ovarian cancer cells to cisplatin via microRNA-93/PTEN/Akt cascade.	tetrahydropalmatine	0-21	microRNA 9-3	Homo sapiens	94-105
31128026-0	2019	L-Tetrahydropalmatine enhances the sensitivity of human ovarian cancer cells to cisplatin via microRNA-93/PTEN/Akt cascade.	Cisplatin	80-89	microRNA 9-3	Homo sapiens	94-105
31128026-2	2019	As miR-93 is reported to be overexpressed in OC and cisplatin resistance, we also evaluated its pathway in OC.	Cisplatin	52-61	microRNA 9-3	Homo sapiens	3-9
31128026-7	2019	Furthermore, we found that the levels of miR-93 in cisplatin-resistant cells were highly expressed compared to parental cells.	Cisplatin	51-60	microRNA 9-3	Homo sapiens	41-47
31128026-8	2019	L-THP suppressed the expression of miR-93 and increased the levels of PTEN, a crucial tumor suppressor in OC.	tetrahydropalmatine	0-5	microRNA 9-3	Homo sapiens	35-41
31128026-11	2019	CONCLUSION: The findings of this study suggested L-THP increased the sensitivity of ovarian cancer cells to cisplatin via modulating miR-93/PTEN/AKT pathway in A2780/DDP ovarian cancer cell line.	tetrahydropalmatine	49-54	microRNA 9-3	Homo sapiens	133-139
31128026-11	2019	CONCLUSION: The findings of this study suggested L-THP increased the sensitivity of ovarian cancer cells to cisplatin via modulating miR-93/PTEN/AKT pathway in A2780/DDP ovarian cancer cell line.	Cisplatin	108-117	microRNA 9-3	Homo sapiens	133-139
30342140-8	2019	Thus, miR-93 may be a potential therapeutic target by GTP for PC therapy.	Guanosine Triphosphate	54-57	microRNA 9-3	Homo sapiens	6-12
30461200-6	2019	The expression of has-miR-30b-5p and has-miR-93-5p was linearly increased across TT, TC, and CC genotypes of rs2241797 in NGT, Ptrend values were 0.024 and 0.016, respectively.	Technetium	85-87	microRNA 9-3	Homo sapiens	41-47
30342533-7	2018	The cluster miR-17-92 (miR-17, miR-20a, miR-20b, and miR-93), along with miR-130, miR-22 and miR-29a/c, were found to differentiate between TNBC and DPBC.	tnbc	140-144	microRNA 9-3	Homo sapiens	53-59
30008789-9	2018	Results: Increased methylation levels of the miR-9-3 promoter region (P < 0.001) and reduced haemoglobin A1C (P < 0.05) were observed in the natural source vitamin E group after intervention.	Vitamin E	162-171	microRNA 9-3	Homo sapiens	45-52
30127988-0	2018	Mechanism of the enhancing effects of miR-93 on resistance of breast cancer MCF-7 cells to adriamycin.	Doxorubicin	91-101	microRNA 9-3	Homo sapiens	38-44
30127988-1	2018	This study aimed to investigate the effects of miR-93 on resistance of breast cancer MCF-7 cells to adriamycin, and to explore the possible mechanism.	Doxorubicin	100-110	microRNA 9-3	Homo sapiens	47-53
30127988-3	2018	miR-93 mimics and inhibitors were transfected into MCF-7/ADM and MCF-7 cells, and MTT assay was used to detect the resistance of cells to adriamycin after transfection.	Doxorubicin	138-148	microRNA 9-3	Homo sapiens	0-6
30127988-12	2018	miR-93 can increase the apoptosis of MCF-7/ADM cells and their resistance to adriamycin by inhibiting the expression of Bcl-2 and P-gp proteins.	Doxorubicin	77-87	microRNA 9-3	Homo sapiens	0-6
30008789-11	2018	Conclusions: alpha-Tocopherol from natural sources increased methylation levels of the miR-9-3 promoter region and reduced haemoglobin A1C in overweight women following an energy-restricted diet.	alpha-Tocopherol	13-29	microRNA 9-3	Homo sapiens	87-94
29525530-0	2018	Sulforaphane epigenetically demethylates the CpG sites of the miR-9-3 promoter and reactivates miR-9-3 expression in human lung cancer A549 cells.	sulforaphane	0-12	microRNA 9-3	Homo sapiens	62-69
29525530-0	2018	Sulforaphane epigenetically demethylates the CpG sites of the miR-9-3 promoter and reactivates miR-9-3 expression in human lung cancer A549 cells.	sulforaphane	0-12	microRNA 9-3	Homo sapiens	95-102
29525530-4	2018	In this study, we aimed to investigate the effect of SFN on restoring the miR-9-3 level in lung cancer A549 cells through epigenetic regulation.	sulforaphane	53-56	microRNA 9-3	Homo sapiens	74-81
29525530-8	2018	We found that CpG methylation was reduced in the miR-9-3 promoter and that miR-9-3 expression was increased after 5 days of treatment with SFN.	sulforaphane	139-142	microRNA 9-3	Homo sapiens	49-56
29525530-8	2018	We found that CpG methylation was reduced in the miR-9-3 promoter and that miR-9-3 expression was increased after 5 days of treatment with SFN.	sulforaphane	139-142	microRNA 9-3	Homo sapiens	75-82
29525530-12	2018	Taken together, these findings indicate that SFN may exert its chemopreventive effects partly through epigenetic demethylation and restoration of miR-9-3.	sulforaphane	45-48	microRNA 9-3	Homo sapiens	146-153