Long noncoding RNA OR3A4 promotes cisplatin resistance of non-small cell lung cancer by upregulating CDK1

J Shang1, Y-D Xu, Y-Y Zhang

  • 1Department of Central Sterile Supply, Yantai Yuhuangding Hospital, Yantai, China. YSLM0142@outlook.com.

Abstract

Insights

Long non-coding RNA OR3A4 promotes cisplatin resistance in non-small cell lung cancer (NSCLC) by upregulating CDK1. Silencing OR3A4 reverses resistance, offering a potential therapeutic target for NSCLC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Long non-coding RNAs (lncRNAs) play a critical role in various cancers, including non-small cell lung cancer (NSCLC).
  • Understanding the specific functions of lncRNAs in drug resistance is crucial for developing effective cancer therapies.

Purpose of the Study:

  • To investigate the role of lncRNA olfactory receptor family 3 subfamily A member 4 (OR3A4) in cisplatin resistance in NSCLC.
  • To explore the underlying molecular mechanisms by which OR3A4 influences cisplatin sensitivity.

Main Methods:

  • Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to measure OR3A4 expression levels.
  • Cell Counting Kit-8 (CCK-8) and flow cytometry were employed to assess the functional impact of OR3A4 on NSCLC cell viability and apoptosis.
  • Mechanism assays were performed to elucidate the molecular pathways involved.

Main Results:

  • OR3A4 expression was significantly higher in cisplatin-resistant NSCLC cells (A549/DDP) compared to sensitive cells (A549).
  • Silencing OR3A4 in A549/DDP cells induced cell cycle arrest and apoptosis, and reversed cisplatin resistance.
  • Knockdown of OR3A4 led to the suppression of CDK1 expression in resistant NSCLC cells.

Conclusions:

  • OR3A4 promotes cisplatin resistance in NSCLC by upregulating CDK1, affecting cell cycle and apoptosis.
  • OR3A4 represents a potential therapeutic target for overcoming cisplatin resistance in non-small cell lung cancer patients.

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