Journal
ONCOTARGETS AND THERAPY
Volume 14, Issue -, Pages 751-761Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/OTT.S240010
Keywords
endometrial cancer; EC; lncRNAs; MCTP1-AS1; miR-650; SMAD7; EMT
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In this study, it was found that MTCP1-AS1 was downregulated in endometrial cancer (EC) tissues and cell lines. Overexpression of MTCP1-AS1 inhibited cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) process in EC cells, potentially through targeting the miR-650/SMAD7 axis.
Background: Long noncoding RNAs (lncRNAs) play critical roles in the pathogenesis of several diseases, especially some kinds of cancer. This study aimed to investigate the expression of MTCP1-AS1 and its effects on endometrial cancer (EC). Methods: MTCP1-AS1 expression level was determined in human EC tissues and cell lines by qRT-PCR. The role of MTCP1-AS1 on EC cell proliferation, migration, invasion and epithelial to mesenchymal transition (EMT) was detected by CCK8, wound-healing assay, transwell assay and Western blot, respectively. Moreover, luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were performed to verify the targeting relationship between miR-650, MCTP1-AS1 and SMAD7 in EC cells. Results: Our data showed that MCTP1-AS1 expression was downregulated in EC tissues and cell lines. Overexpression of MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells. Moreover, MCTP1-AS1 was proved to be the target of miR-650 and reversely correlated with its expression. In addition, MCTP1-AS1 reversed the effect of miR-650 on the EC cells, which might be associated with the role of SMAD7. Moreover, Western blot showed siRNA-SMAD7 transfection could rescue the repressed TGF-beta/SMAD pathway induced by MCTP1-AS1 in EC cells. Conclusion: Taken together, these data suggested that lncRNA MCTP1-AS1 inhibited cell proliferation, migration, invasion and EMT process of EC cells via targeting the miR-650/SMAD7 axis and it has the potential to be explored as a therapeutic target for the treatment of EC in the future.
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