Abstract
LncRNA LINC01518 was previously reported to be upregulated in oesophageal squamous cell carcinoma (ESCC) tissues compared with normal tissues. However, there are no previous studies concerning the specific function and molecular mechanism of LINC01518 in ESCC. LINC01518 and miR-1-3p expression levels in ESCC cells were detected by qRT-PCR. Cell proliferation and apoptosis were evaluated by CCK-8 and flow cytometry analysis, respectively. The relationships between LINC01518, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA) and miR-1-3p were explored by luciferase reporter assay. The alteration of the PIK3CA/protein kinase B (Akt) pathway was examined by Western blot. We found that LINC01518 expression was upregulated and miR-1-3p expression was downregulated in ESCC cells. LINC01518 knockdown inhibited cell proliferation and promoted apoptosis in ESCC cells. In addition, LINC01518 functioned as a competing endogenous RNA (ceRNA) for miR-1-3p in ESCC cells and miR-1-3p downregulation blocked the effects of LINC01518 knockdown on cell proliferation and apoptosis in ESCC cells. Moreover, PIK3CA was identified as a target of miR-1-3p and LINC01518 knockdown inhibited the PIK3CA/Akt pathway by upregulating miR-1-3p in ESCC cells. In conclusion, LINC01518 knockdown inhibited tumorigenicity in ESCC cells by suppression of PIK3CA/Akt pathway through upregulating miR-1-3p.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.