Knockdown of miR-214 promotes apoptosis and inhibits cell proliferation in nasopharyngeal carcinoma.
Ontology highlight
ABSTRACT:
SUBMITTER: Zhang ZC
PROVIDER: S-EPMC3897649 | biostudies-literature | 2014
REPOSITORIES: biostudies-literature
Publications
Knockdown of miR-214 promotes apoptosis and inhibits cell proliferation in nasopharyngeal carcinoma.
Zhang Zi-Chen ZC Li Yang-Yang YY Wang Hai-Yun HY Fu Sha S Wang Xiao-Pai XP Zeng Mu-Sheng MS Zeng Yi-Xin YX Shao Jian-Yong JY
PloS one 20140121 1
MicroRNA-214 (MiR-214) is aberrantly expressed in several human tumors such as ovarian cancer and breast cancer. However, the role of miR-214 in nasopharyngeal carcinoma (NPC) is still unknown. In this study, we report that miR-214 was overexpressed in NPC cell lines and tissues. Silencing of miR-214 by LNA-antimiR-214 in NPC cells resulted in promoting apoptosis and suppressing cell proliferation in vitro, and suppressed tumor growth in nude mice in vivo. Luciferase reporter assay was performed ...[more]
Similar Datasets
Project description:Previous studies have reported that scinderin (SCIN) affects multiple cellular processes, including proliferation, migration and differentiation in cancer. However, the specific role of SCIN in breast cancer (BC) cells is unknown. Immunohistochemistry was used to investigate SCIN expression in 46 BC and 21 mammary fibroadenoma or fibroadenomatoid hyperplasia tissue samples. SCIN expression was ablated in MDA-MB-231 and T-47D cells using lentivirus-mediated small interfering RNA technology. Cell proliferation was tested using Celigo and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays. Cell apoptosis was analyzed by measuring Caspase 3/7 activity and annexin-V staining. The results of the present study demonstrated that SCIN expression was elevated in BC tissues compared with mammary fibroadenoma or fibroadenomatoid hyperplasia tissues. Specifically, higher SCIN expression was observed in Ki-67-positive BC tissues (78.6%) compared with Ki-67-negative BC tissues. Furthermore, knockdown of SCIN expression in the BC cell lines significantly suppressed cell proliferation and induced apoptosis. The data presented in the present study indicate that SCIN serves an important role in the development of breast cancer.
| S-EPMC6096137 | biostudies-literature
Project description:BackgroundThe incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide.ObjectivesAlthough previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma.Materials and methodsReal-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression.ResultsThe expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT).ConclusionmiRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway.SignificanceThe role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.
| S-EPMC6985969 | biostudies-literature
Project description:Introduction:MCM3AP-AS1 has been characterized as an oncogenic lncRNA in several types of cancer, while its role in nasopharyngeal carcinoma (NPC) is unknown. This study aimed to investigate the role of MCM3AP-AS1 in NPC. Patients and Methods:Paired NPC tissues and non-tumor tissues were collected from 55 NPC patients. Expression of MCM3AP-AS1 and miR-34a in paired tissues was analyzed by RT-qPCR. Interactions between MCM3AP-AS1 and miR-34a were analyzed by overexpression experiments. The roles of MCM3AP-AS1 and miR-34a in regulating NPC cell proliferation and apoptosis were explored by cell proliferation assay and cell apoptosis assay, respectively. Results:Our bioinformatics analysis showed that MCM3AP-AS1 may be targeted by miR-34a, which is a well-studied tumor suppressor miRNA. In this study, we showed that miR-34a was downregulated and MCM3AP-AS1 was upregulated in NPC. An inverse correlation between the expression of MCM3AP-AS1 and miR-34a was found across NPC tissue samples. High expression level of MCM3AP-AS1 and low levels of miR-34a in NPC tissues predicted the poor survival. In NPC cells, overexpression of MCM3AP-AS1 did not affect the expression of miR34a, while overexpression of miR-34a led to downregulated MCM3AP-AS1. Cell proliferation and apoptosis assay showed that overexpression of miR-34a reduced the enhancing effects of overexpressing MCM3AP-AS1 on cell proliferation and the inhibitory effects on cell apoptosis. Conclusion:MiR-34a inhibits cell proliferation and induces apoptosis in human NPC by targeting MCM3AP-AS1.
| S-EPMC7319531 | biostudies-literature
Project description:Nasopharyngeal carcinoma (NPC) is often associated with the infection of Epstein-Barr virus in nasopharynx and is mainly happened in South China and Southeast Asia. Recently, noncoding RNAs have been reported to regulate NPC carcinogenesis. LncRNA OIP5-AS1 participates in tumorigenesis and progression; however, the inherent mechanism of OIP5-AS1-mediated progression of NPC is unclear. In the current study, we aimed to explore the role of OIP5-AS1 in NPC progression. We measured the cell viability, apoptosis, migration, and invasion in NPC cells after OIP5-AS1 modulation. Moreover, we determined whether OIP5-AS1 exerts its oncogenic functions via sponging miR-183-5p in NPC. Furthermore, we determined whether glutamate ammonia ligase (GLUL) was a downstream target of miR-183-5p. We found that OIP5-AS1 downregulation inhibited the viability, migration and invasion of NPC via targeting miR-183-5p. We also identified that GLUL might be a potential downstream target of miR-183-5p in NPC cells. Mechanistically, OIP5-AS1 promotes cell motility via regulating miR-183-5p and GLUL in NPC cells. We concluded that OIP5-AS1 performed its biological functions via targeting miR-183-5p and GLUL in NPC cells.
| S-EPMC9214031 | biostudies-literature
Project description:BackgroundCervical cancer (CC) is one of the most common gynaecological malignancies all around the world. The mechanisms of cervical carcinoma formation remain under close scrutiny. The long non-coding RNAs (lncRNA) and microRNAs (miRNAs) play important roles in controlling gene expression and promoting the development and progression of cervical cancer by acting as competitive endogenous RNA (ceRNA). However, the roles of lncRNA associated with ceRNAs in cervical carcinogenesis remains unknown. In this study, the expression of long non-coding RNA HOTAIR was investigated in HPV16 positive cervical cancer cells, the candidate miRNAs and target genes were identified to clarify putative ceRNAs of HOTAIR/miRNA in cervical cancer cells.MethodsThe proliferation ability of cells was measured by CCK8 and EdU incorporation assays and cell apoptosis was analyzed by flow cytometry. The expression of HOTAIR, miR-214-3p, HPV16 E7 mRNA were detected by qRT-PCR. As for searching for the interaction between miR-214-3p and HOTAIR, the binding sites for miR-214-3p on HOTAIR was predicted by starbase v2.0 database, then dual-luciferase assay was used to verify the binding sites. In addition, Gene Ontology (GO) and protein-protein interaction (PPI) network analysis of target genes of miR-214-3p were performed with bioinformatics analysis. The potential signal pathway regulated by HOTAIR/miR-214-3p was predicted by KEGG enrichment analysis and confirmed by qPCR and WB analysis in cervical cancer cells.ResultsOur results showed that expression of HOTAIR was up-regulated, while that of miR-214-3p was down-regulated in HPV16-positive cervical cancer cells. The expression status of HPV16 E7 played an important role in regulating expression of HOTAIR or miR-214-3p in cervical cancer cells. HOTAIR knockdown could significantly inhibited cell proliferate ability and promote cellular apoptosis, whereas the inhibition of miR-214-3p expression partially reversed such results. Bioinformatics analysis identified 1451 genes as target genes of miR-214-3p. The Gene ontology (GO) and KEGG Pathway enrichment analysis showed that these target genes were mainly related to regulation of cell communication, protein binding, enzyme binding and transferase activity, and Wnt ligand biogenesis. Pathway enrichment analysis results showed that the predicted target genes were significantly enriched in Wnt/β-catenin signaling pathway. Finally, our results confirmed that miR-214-3p could significantly inhibit β-catenin expression in HPV16 positive cancer cells by qPCR and WB analysis.ConclusionHOTAIR could act as a ceRNA through binding to miR-214-3p, promote cell proliferation and inhibit the apoptosis of HPV16 positive cervical cancer. HOTAIR/miR-214-3p/Wnt/β-catenin signal pathway might played important regulated roles in HPV16 positive cervical cancer. Our results provided new insight into defining novel biomarkers for cervical cancer.
| S-EPMC8317292 | biostudies-literature
Project description:Background:Colorectal cancer (CRC) is one of the leading causes of cancer-related death worldwide. Increasing evidence showed that circular RNAs (circRNAs) played critical roles in the progression of CRC. However, the effects and underlying mechanisms of circ_0000512 in CRC progression remain unclear. Methods:The expression levels of circ_0000512, microRNA-296-5p (miR-296-5p) and runt-related transcription factor 1 (RUNX1) were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, colony formation, cell cycle distribution and cell apoptosis were detected by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and flow cytometry analysis, respectively. Western blot assay was utilized to measure the protein expression of Cyclin D1, Cleaved Caspase-3 and RUNX1. The interaction between miR-296-5p and circ_0000512 or RUNX1 was predicted by starBase and verified by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull-down assay. The mice xenograft model was established to explore the function of circ_0000512 in vivo. Results:The expression of circ_0000512 was increased in CRC tissues and cells. Knockdown of circ_0000512 suppressed cell viability and colony formation and arrested the cells at the G0/G1 phase while it accelerated apoptosis in CRC cells. Mechanistically, circ_0000512 could increase RUNX1 expression by acting as a molecular sponge of miR-296-5p in CRC cells. Furthermore, miR-296-5p downregulation or RUNX1 overexpression reversed the anti-proliferation and pro-apoptosis effects caused by circ_0000512 knockdown in CRC cells. In addition, circ_0000512 interference inhibited tumor growth by upregulating miR-296-5p and downregulating RUNX1 in vivo. Conclusion:Knockdown of circ_0000512 inhibited cell proliferation and induced apoptosis in CRC cell by regulating miR-296-5p/RUNX1 axis, which might provide a potential therapeutic target for CRC treatment.
| S-EPMC7419622 | biostudies-literature
Project description:BackgroundIncreasing evidence indicates that the dysregulation of miRNAs plays a vital role in tumorigenesis and progression of nasopharyngeal carcinoma (NPC). Thus, it is necessary to further investigate the function and mechanism of miRNAs in NPC.MethodsmiR-100 expression was analyzed using publicly available databases and then tested using quantitative RT-PCR in NPC tissues and cell lines. MTT and colony formation assays and xenograft tumor model were used to test the NPC cell growth and proliferation abilities while modulating miR-100 expression. The target of miR-100 was predicted with TargetScan and validated with luciferase reporter assay, quantitative RT-PCR, and Western blot.ResultsThe expression of miR-100 was significantly reduced in NPC tissues and cell lines. Overexpression of miR-100 obviously suppressed NPC cell growth and proliferation, whereas silencing miR-100 promoted NPC cell growth and proliferation in vitro. HOXA1 (homeobox A1) was validated as a direct target of miR-100, and restoring HOXA1 expression could reverse the inhibitive effect of miR-100 on NPC cell growth and proliferation. The mRNA and protein expression of HOXA1 was increased in NPC cell lines. Furthermore, ectopic expression of miR-100 inhibited xenograft tumor growth in vivo.ConclusionTaken together, our findings suggest that miR-100 could suppress NPC growth and proliferation through targeting HOXA1, providing a novel target for the miRNA-mediated therapy for patients with NPC in the future.
| S-EPMC6980857 | biostudies-literature
Project description:Non-small cell lung cancer, as the most frequent type lung cancer, has lower survival rate of 5 years, despite improvements in surgery and chemotherapy. Previous studies showed immature colon carcinoma transcript 1 is closely related to tumorigenesis of human cancer cells. In the present study, we found immature colon carcinoma transcript 1 was overexpressed in lung cancer tissues using Oncomine database mining, and the biological effect of immature colon carcinoma transcript 1 was investigated in non-small cell lung cancer cell lines 95D and A549. Lentivirus-mediated RNA interference was used to knock down immature colon carcinoma transcript 1 expression in 95D and A549 cells in vitro, and the knockdown efficiency was determined using quantitative real-time polymerase chain reaction and Western blot assay. Knockdown of immature colon carcinoma transcript 1 significantly suppressed non-small cell lung cancer cell proliferation and colony formation ability confirmed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Flow cytometry was applied to measure cell cycle arrest, and the result showed the cell cycle arrested in G2/M phase in 95D cells and arrested in G0/G1 phase in A549 cells. Furthermore, we measured the levels of cell cycle-associated proteins by Western blot analysis and found immature colon carcinoma transcript 1 -mediated cell proliferation inhibition appeared due to downregulation of cell cycle activator cyclin D1 and upregulation of cell cycle inhibitor p21. In addition, immature colon carcinoma transcript 1 silencing significantly induced non-small cell lung cancer cell apoptosis by annexin V/7-amino-actinomycin D double-staining assay. All our data suggest that immature colon carcinoma transcript 1 may play an important role for non-small cell lung cancer cell proliferation and could be a potential molecular target for diagnosing and treating human non-small cell lung cancer.
| S-EPMC5665147 | biostudies-literature
Project description:The v-Crk avian sarcoma virus CT10 oncogene homolog-like (CRKL) protein is important in cancer progression. However, its expression pattern and biological roles in human endometrial carcinoma remain unexplored. The potential mechanism of CRKL-induced cancer progression is still unclear. The present study aimed to explore the expression pattern and biological roles of CRKL in human endometrial carcinoma. Using immunohistochemistry, it was observed that the CRKL protein was overexpressed in 50.5% (44/87) of endometrial carcinoma tissues. Plasmid transfection of CRKL into Ishikawa cells was performed, and CRKL overexpression promoted cell proliferation, colony formation and cell cycle transition in the transfected cells. In addition, CRKL overexpression inhibited cell apoptosis in Ishikawa cells treated with cisplatin, with decreased caspase-3 and caspase-9 cleavage. Further analysis revealed that CRKL upregulated the expression of cyclin D1, cyclin E, B cell lymphoma (Bcl)-2 and survivin, and downregulated Bcl-2 associated X protein expression. In conclusion, the present study demonstrated that CRKL overexpression in endometrial carcinoma contributes to malignant cell growth and resistance to apoptosis, possibly through Bcl-2.
| S-EPMC5245097 | biostudies-literature
Project description:MicroRNAs (miRNAs) may act as either tumor suppressors or oncogenes in various types of cancers. Previous studies have indicated that miR-17-5p is involved in the initiation and development of human tumors. However, its mechanism and function in nasopharyngeal carcinoma (NPC) remain largely unclear. In this study, we evaluated the expression profiles of miR-17-5p and p21 in NPC cell lines and tissues by quantitative real-time PCR (qRT-PCR). For the analysis, we have established a stable overexpression or depletion of miR-17-5p NPC cell lines for analyzing the effects of cell proliferation by MTT, colony formation, and cell cycle assay. A nude mice xenograft model was used to verify the tumor growth in vivo. MiR-17-5p was overexpressed, whereas the expression of p21 was downregulated in NPC cell lines and tissues. The miR-17-5p expression level was inversely correlated with the p21 mRNA level in NPC samples. Furthermore, analysis of 2-??Ct value in 81 NPC patients suggested that the elevated expression level of miR-17-5p or the downregulated expression level of p21 was significantly correlated with tumor size (T classification) and tumor stage, and Kaplan-Meier survival analysis revealed a correlation between miR-17-5p or p21 expression level and overall survival times in 81 NPC patients. MiR-17-5p promoted cell growth in vivo and in vitro by directly targeting p21. Our results indicate that miR-17-5p can promote the occurrence of NPC and it may serve as a potential novel diagnostic maker or therapeutic target for NPC in the future.
| S-EPMC5224848 | biostudies-other