MicroRNA-25-3p promotes cisplatin resistance in Non-small-cell lung carcinoma (NSCLC) through adjusting PTEN/PI3K/AKT

Butong Sun1, Nanjun Hu1, Dan Cong1

  • 1Department of Hematology and Oncology, China-Japan Union Hospital of Jilin University, Changchun City, China.

Bioengineered
|July 16, 2021
PubMed

Insights

MicroRNA miR-25-3p increases cisplatin resistance in non-small cell lung cancer (NSCLC). Targeting this microRNA and the PTEN/PI3K/AKT pathway may overcome chemotherapy resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Drug resistance is a major challenge in non-small cell lung cancer (NSCLC) treatment.
  • MicroRNAs play significant roles in regulating cellular processes, including drug resistance.

Purpose of the Study:

  • To investigate the role of miR-25-3p in cisplatin (DDP) resistance in NSCLC.
  • To elucidate the underlying molecular mechanisms, including the PTEN/PI3K/AKT pathway.

Main Methods:

  • Quantitative real-time PCR (RT-qPCR) for miR-25-3p expression.
  • Cell viability (MTS assay), colony formation, apoptosis (Annexin V/PI), and invasion (Transwell) assays.
  • Luciferase reporter, Western blot, and in vivo tumor growth studies.

Main Results:

  • miR-25-3p expression was elevated in cisplatin-resistant NSCLC cells.
  • miR-25-3p mimic enhanced DDP resistance, invasion, and metastasis, activating the PTEN/PI3K/AKT pathway.
  • PTEN was identified as a direct target of miR-25-3p; PTEN inhibition mimicked miR-25-3p effects.
  • In vivo studies confirmed miR-25-3p promotes tumor growth and DDP resistance.

Conclusions:

  • The miR-25-3p/PTEN/PI3K/AKT axis promotes cisplatin resistance in NSCLC.
  • This axis represents a potential therapeutic target for overcoming chemotherapy resistance in NSCLC.

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