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High-resolution Respirometry to Assess Mitochondrial Function in Permeabilized and Intact Cells
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miR-663 sustains NSCLC by inhibiting mitochondrial outer membrane permeabilization (MOMP) through PUMA/BBC3 and BTG2

Micol E Fiori1,2, Lidia Villanova3, Chiara Barbini3

  • 1Institute of General Pathology, Catholic University of the Sacred Heart and Gemelli Polyclinic, Rome, Italy. fiorimicol@gmail.com.

Cell Death & Disease
|January 21, 2018
PubMed

Insights

MicroRNA-663 (miR-663) promotes non-small cell lung cancer (NSCLC) growth by inhibiting apoptosis. Targeting miR-663 effectively triggers cancer cell death and reduces tumor growth, offering a potential new therapy for lung cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Lung cancer remains a leading cause of cancer mortality worldwide, necessitating novel therapeutic strategies.
  • MicroRNAs (miRNAs) are frequently dysregulated in cancer and represent promising targets for therapeutic intervention.
  • Identifying specific miRNAs involved in non-small cell lung cancer (NSCLC) pathogenesis is crucial for developing new treatments.

Purpose of the Study:

  • To investigate the oncogenic role of miR-663 in NSCLC.
  • To explore the therapeutic potential of targeting miR-663 in NSCLC.

Main Methods:

  • Utilized high-content screening to identify miRNAs regulating NSCLC proliferation.
  • Performed miR-663 knockdown experiments in NSCLC cells.
  • Analyzed the impact of miR-663 modulation on apoptosis and tumor growth in vitro and in vivo.
  • Investigated direct targets of miR-663, including PUMA/BBC3 and BTG2.

Main Results:

  • miR-663 was identified as an oncogenic miRNA in NSCLC.
  • miR-663 regulates apoptosis by controlling mitochondrial outer membrane permeabilization (MOMP).
  • miR-663 targets PUMA/BBC3 and BTG2, influencing cell death pathways.
  • Depletion of miR-663 induced apoptosis in NSCLC cells and inhibited tumor growth in vivo.

Conclusions:

  • miR-663 plays a significant role in NSCLC progression by suppressing apoptosis.
  • Targeting miR-663 presents a viable therapeutic strategy for NSCLC treatment.
  • Modulating miR-663 can induce cancer cell death and impair tumor growth, highlighting its potential clinical relevance.

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