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miR-496 suppress tumorigenesis via targeting BDNF-mediated PI3K/Akt signaling pathway in non-small cell lung cancer

Rui Ma1, Pan Zhu2, Shu Liu3

  • 1Department of Integrated Medicine, Affiliated to Dongfeng Hospital, Hubei University of Medicine, Shiyan, Hubei, China.

Biochemical and Biophysical Research Communications
|August 19, 2019
PubMed

Insights

MicroRNA-496 (miR-496) inhibits non-small cell lung cancer (NSCLC) growth by targeting Brain-Derived Neurotrophic Factor (BDNF). This study reveals miR-496

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Abnormal microRNA-496 (miR-496) expression is observed in non-small cell lung cancer (NSCLC).
  • The precise role and mechanism of miR-496 in NSCLC tumorigenesis require further elucidation.

Purpose of the Study:

  • To investigate the function of miR-496 in NSCLC development.
  • To identify the molecular mechanism underlying miR-496's action in NSCLC.

Main Methods:

  • Bioinformatic analysis was employed to identify potential targets of miR-496.
  • The expression of miR-496 and its target were analyzed in NSCLC patients and cell lines.
  • Functional assays were performed to assess the impact of miR-496 on cell proliferation and signaling pathways.

Main Results:

  • Increased miR-496 expression significantly suppressed NSCLC cell proliferation in vitro and in vivo.
  • Brain-Derived Neurotrophic Factor (BDNF) was identified as a direct target of miR-496.
  • miR-496 inactivated the BDNF-mediated PI3K/Akt signaling pathway, thereby inhibiting tumor growth.

Conclusions:

  • miR-496 functions as a tumor suppressor in NSCLC.
  • The miR-496/BDNF axis plays a critical role in regulating NSCLC progression.
  • Targeting miR-496 may represent a potential therapeutic strategy for NSCLC.
Keywords:
Brain derived neurotrophic factorNon-small cell lung cancerPI3K/Akt signaling pathwaymicroRNA-496

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