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STAT3/miR-135b/NF-κB axis confers aggressiveness and unfavorable prognosis in non-small-cell lung cancer

Jinlin Zhao1, Xin Wang1, Zeyun Mi2

  • 1Department of Radiation Oncology, Tianjin Medical University Cancer Institute & Hospital, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center for Cancer, Tianjin's Clinical Research Center for Cancer, 300060, Tianjin, China.

Cell Death & Disease
|May 15, 2021
PubMed

Insights

MicroRNA-135b (miR-135b) promotes non-small-cell lung cancer (NSCLC) aggressiveness by targeting CYLD and activating NF-κB signaling. This miR-135b upregulation offers a potential therapeutic target for NSCLC treatment.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Non-small-cell lung cancer (NSCLC) presents limited therapeutic options, necessitating research into its pathological and molecular mechanisms.
  • MicroRNAs (miRNAs) are implicated in cancer development, including NSCLC, making them targets for investigation.

Purpose of the Study:

  • To identify novel microRNAs involved in NSCLC progression.
  • To elucidate the role and mechanism of microRNA-135b (miR-135b) in NSCLC.

Main Methods:

  • Quantitative real-time PCR to measure miR-135b levels in NSCLC tissues.
  • In vitro and in vivo assays to assess the impact of miR-135b overexpression and knockdown on NSCLC aggressiveness.
  • Luciferase reporter assays and Western blotting to investigate the molecular targets and signaling pathways affected by miR-135b.

Main Results:

  • miR-135b was significantly upregulated in NSCLC and correlated with poor patient prognosis, acting as an independent prognostic factor.
  • Overexpression of miR-135b enhanced NSCLC cell proliferation, migration, invasion, anti-apoptosis, and angiogenesis, while knockdown yielded opposite effects.
  • miR-135b directly targets the 3'-UTR of CYLD, modulating NF-κB signaling. The IL-6/STAT3 pathway upregulates miR-135b, forming a positive feedback loop.

Conclusions:

  • miR-135b acts as a tumor promoter in NSCLC by regulating the CYLD/NF-κB axis.
  • A positive feedback loop involving IL-6/STAT3/miR-135b/NF-κB signaling contributes to NSCLC progression.
  • miR-135b represents a promising therapeutic target for NSCLC treatment.

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