LncRNA MCTP1-AS1 Regulates EMT Process in Endometrial Cancer by Targeting the miR-650/SMAD7 Axis
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). MTCP1-AS1 expression level was determined in human EC tissues and cell l...
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Veröffentlicht in: | OncoTargets and therapy 2021-01, Vol.14, p.751-761 |
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Zusammenfassung: | 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).
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.
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-β/SMAD pathway induced by MCTP1-AS1 in EC cells.
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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ISSN: | 1178-6930 1178-6930 |
DOI: | 10.2147/OTT.S240010 |