AI Article Synopsis

  • Long non-coding RNA LINC00847 is shown to be upregulated in non-small cell lung cancer (NSCLC) and is associated with poor prognosis in patients.
  • Research methods included RT-qPCR, cell tests, a xenograft tumor model, and molecular assays to investigate LINC00847's role in cell proliferation and metastasis.
  • The findings suggest that E2F1 promotes LINC00847 expression, which in turn regulates the miR-147a/IFITM1 axis, contributing to NSCLC progression.

Article Abstract

Long non-coding RNAs (lncRNAs) can remarkably regulate human malignancies in terms of the development and the progression. Previously, lncRNA LINC00847 (LINC00847) has been reported to present dysregulation in several tumors. However, the expression and function of LINC00847 in non-small cell lung cancer (NSCLC) have not been investigated. RT-qPCR was performed to determine the expressions of LINC00847 in collected tissue samples and cell lines. The clinical significance of LINC00847 was statistically analyzed. CCK-8 test, cell scratch test and trans-well test were used to evaluate the proliferation, invasion and migration abilities of NSCLC cells, respectively. The xenograft tumor model was constructed to confirm the effects of LINC00847 knockdown on NSCLC . Further, luciferase reporter assays and Western blot were performed to explore molecular mechanisms underlying the functions of LINC00847. Increased expressions of LINC00847 were observed in NSCLC samples as well as cell lines. Additionally, E2F1 could be capable of directly binding to the LINC00847 promoter region, followed by promoting its expression. Clinically, LINC00847 high-expression could lead to poor prognosis of NSCLC patients. Functionally, LINC00847 knockdown noticeably repressed NSCLC cell growth and metastasis. Mechanically, miR-147a/IFITM1 axis was a downstream target of LINC00847, and silencing of miR-147a could rescue the anti-cancer effects of LINC00847 knockdown on NSCLC cell behaviors. Overall, up regulation of LINC00847 induced by E2F1 promoted the progression of NSCLC by modulating miR-147a/IFITM1 axis, representing a novel regulatory mechanism for NSCLC progression.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8100058PMC
http://dx.doi.org/10.3389/fmed.2021.663558DOI Listing

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