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miR-326 reverses chemoresistance in human lung adenocarcinoma cells by targeting specificity protein 1

Jipeng Li1, Shanfeng Li1, Zhe Chen1

  • 1Department of Central Laboratory, Yinzhou People's Hospital, Ningbo, 315040, China.

Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine
|July 28, 2016
PubMed

Insights

MicroRNA-326 (miR-326) downregulation contributes to cisplatin resistance in lung adenocarcinoma (LAD). Restoring miR-326 or targeting SP1 can overcome this resistance, revealing a novel therapeutic pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cisplatin resistance is a significant challenge in treating lung adenocarcinoma (LAD).
  • The underlying mechanisms of cisplatin resistance in LAD remain incompletely understood.
  • Identifying novel molecular targets is crucial for improving chemotherapy efficacy.

Purpose of the Study:

  • To investigate the role of microRNA-326 (miR-326) in cisplatin resistance in LAD.
  • To identify the direct targets of miR-326 involved in chemoresistance.
  • To explore the involvement of HOTAIR in regulating chemoresistance via the miR-326/SP1 pathway.

Main Methods:

  • Comparison of miR-326 expression in cisplatin-resistant (A549/CDDP) and parental (A549) LAD cells.
  • In vitro and in vivo experiments involving overexpression of miR-326 and knockdown of SP1.
  • Identification of SP1 as a direct target of miR-326 using bioinformatics and experimental validation.
  • Analysis of miR-326 and SP1 expression in tumor tissues from LAD patients undergoing cisplatin-based chemotherapy.
  • Investigation of HOTAIR's role in modulating the miR-326/SP1 pathway.

Main Results:

  • miR-326 was significantly downregulated in cisplatin-resistant LAD cells.
  • Overexpression of miR-326 restored sensitivity to cisplatin in LAD cells both in vitro and in vivo.
  • SP1 was identified as a direct target of miR-326, and its knockdown mimicked the effects of miR-326 overexpression.
  • Decreased miR-326 and increased SP1 expression correlated with reduced cisplatin sensitivity in patient tumor tissues.
  • Repression of HOTAIR partially reversed chemoresistance by modulating the miR-326/SP1 pathway.

Conclusions:

  • miR-326 plays a critical role in regulating cisplatin chemoresistance in LAD.
  • The HOTAIR/miR-326/SP1 axis represents a novel pathway influencing chemoresistance in LAD.
  • Targeting the miR-326/SP1 pathway offers a potential therapeutic strategy to overcome cisplatin resistance in LAD.
Keywords:
ChemoresistanceHOTAIRLung adenocarcinomaSP1miR-326

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