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Silencing lncRNA MCM3AP-AS1 protects against cisplatin-induced cell death in A549 lung cancer cells

Ibrahim Bozgeyik1, Demet Tasdemir2,3, Esra Bozgeyik4

  • 1Department of Medical Biology, Faculty of Medicine, Adiyaman University, 02040, Adiyaman, Turkey. i.bozgeyik@gmail.com.

Molecular Biology Reports
|July 14, 2025
PubMed
Abstract

Insights

Long non-coding RNA MCM3AP-AS1 is upregulated in lung cancer cells treated with cisplatin. Silencing MCM3AP-AS1 increases cell viability and decreases apoptosis, suggesting its role in cisplatin resistance.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genetics

Background:

  • Lung cancer is a leading cause of cancer mortality globally.
  • Cisplatin resistance is a major challenge in lung cancer treatment.
  • Long non-coding RNAs (lncRNAs) are implicated in drug resistance mechanisms.

Purpose of the Study:

  • To investigate the role of MCM3AP-AS1 in cisplatin-induced cell death in lung cancer.
  • To determine if MCM3AP-AS1 influences cisplatin resistance in lung cancer cells.

Main Methods:

  • Upregulation of MCM3AP-AS1 in A549 lung cancer cells after cisplatin treatment was observed.
  • RNA interference was used to silence MCM3AP-AS1 expression.
  • Cell viability was assessed using MTT assay.
  • Apoptosis was measured by Annexin V/PI flow cytometry and acridine orange/ethidium bromide staining.

Main Results:

  • MCM3AP-AS1 was significantly upregulated in lung cancer cells following cisplatin treatment.
  • Silencing MCM3AP-AS1 led to increased cell viability.
  • Knockdown of MCM3AP-AS1 resulted in decreased apoptosis in response to cisplatin.

Conclusions:

  • MCM3AP-AS1 plays a significant role in mediating resistance to cisplatin-induced apoptosis in lung cancer.
  • MCM3AP-AS1 may serve as a potential therapeutic target for overcoming cisplatin resistance in lung cancer.
Keywords:
CancerCisplatinLncRNALung cancerMCM3AP-AS1

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