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Published on: April 10, 2018

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Long noncoding RNA NEAT1 aggravates sorafenib-resistance in non-small cell lung cancer via regulating miRNA-335/c-Met

Lin Mu1, Hong Zhao, Yayun Yang

  • 1Department of Pulmonary and Critical Care Medicine, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, China.

Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology
|June 2, 2021
PubMed
Abstract

Insights

Long non-coding RNA NEAT1 promotes sorafenib resistance in non-small cell lung cancer (NSCLC) by inhibiting microRNA-335 (miR-335) and upregulating c-Met. Silencing NEAT1 enhances sorafenib sensitivity, reducing proliferation and increasing apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Non-small cell lung cancer (NSCLC) exhibits resistance to targeted therapies like sorafenib.
  • Long non-coding RNAs (lncRNAs) play crucial roles in cancer progression and drug resistance.
  • Investigating molecular mechanisms underlying sorafenib resistance is vital for improving NSCLC treatment.

Purpose of the Study:

  • To elucidate the role of lncRNA NEAT1 in modulating sorafenib sensitivity in NSCLC.
  • To investigate the NEAT1/microRNA-335 (miR-335)/c-Met signaling axis in this context.
  • To understand how NEAT1 influences proliferation and apoptosis in sorafenib-treated NSCLC cells.

Main Methods:

  • Cell Counting Kit-8 (CCK-8) and colony formation assays assessed cell proliferation.
  • Apoptosis rates and Bcl-2/Bax levels were analyzed to evaluate apoptosis.
  • Dual-luciferase reporter gene assays confirmed interactions within the NEAT1/miR-335/c-Met pathway.

Main Results:

  • Silencing NEAT1 significantly enhanced sorafenib-induced apoptosis and attenuated proliferation in NSCLC cells (A549 and PC9).
  • NEAT1 was identified as a negative regulator of miR-335, and miR-335 directly targeted c-Met.
  • Rescue experiments confirmed the NEAT1/miR-335/c-Met loop's role in mediating sorafenib resistance.

Conclusions:

  • LncRNA NEAT1 exacerbates sorafenib resistance in NSCLC by inhibiting miR-335, leading to c-Met upregulation.
  • This mechanism results in reduced proliferation and increased apoptosis in response to sorafenib.
  • Targeting the NEAT1/miR-335/c-Met axis may represent a therapeutic strategy to overcome sorafenib resistance in NSCLC.

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