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MiR-124 changes the sensitivity of lung cancer cells to cisplatin through targeting STAT3

M-M Qi1, F Ge, X-J Chen

  • 1School of Basic Medicine, Nanjing University of Chinese Medicine, Nanjing, China. 718171345@qq.com.

European Review for Medical and Pharmacological Sciences
|July 13, 2019
PubMed
Abstract

Insights

MicroRNA-124 (miR-124) is downregulated in non-small cell lung cancer (NSCLC) drug resistance. Restoring miR-124 enhances cisplatin sensitivity and inhibits NSCLC cell invasion and metastasis by targeting STAT3.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Drug resistance in non-small cell lung cancer (NSCLC) poses a significant clinical challenge.
  • MicroRNAs (miRNAs) play crucial roles in cancer progression and drug response.
  • The specific role of miR-124 in NSCLC chemoresistance remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of microRNA-124 (miR-124) in the development of drug resistance in non-small cell lung cancer (NSCLC).
  • To explore the underlying molecular mechanism by which miR-124 influences NSCLC chemoresistance.
  • To assess miR-124's potential as a therapeutic target for overcoming cisplatin resistance in NSCLC.

Main Methods:

  • Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting were used to measure miR-124 and STAT3 expression levels in NSCLC cells.
  • Cell lines were transfected with miR-124 mimics to overexpress miR-124.
  • Cellular sensitivity to cisplatin, apoptosis, invasion, and metastasis were assessed using MTT assays, flow cytometry, wound healing, and Transwell assays, respectively. Luciferase reporter gene assays were employed to confirm the interaction between miR-124 and STAT3.

Main Results:

  • Expression of miR-124 was significantly lower, while signal transducer and activator of transcription 3 (STAT3) expression was significantly higher in cisplatin-resistant NSCLC cells (A549/DDP) compared to sensitive cells (A549).
  • Overexpression of miR-124 in A549/DDP cells reduced STAT3 expression, enhanced sensitivity to cisplatin, and inhibited cell invasion and metastasis.
  • Luciferase reporter assays confirmed that miR-124 directly targets the 3'-untranslated region (UTR) of STAT3, leading to its negative regulation.

Conclusions:

  • MiR-124 plays a critical role in regulating the sensitivity of non-small cell lung cancer (NSCLC) to cisplatin chemotherapy.
  • MiR-124 inhibits NSCLC cell invasion and metastasis by targeting and downregulating STAT3 expression.
  • STAT3 represents a potential therapeutic target for overcoming cisplatin resistance in NSCLC, with miR-124 serving as a key regulator in this process.

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