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miR-300 regulates cellular radiosensitivity through targeting p53 and apaf1 in human lung cancer cells

Jinpeng He1, Xiu Feng1,2, Junrui Hua1

  • 1a Key Laboratory of Space Radiobiology of Gansu Province & Key Laboratory of Heavy Ion Radiation Biology and Medicine, Institute of Modern Physics , Chinese Academy of Sciences , Lanzhou , China.

Cell Cycle (Georgetown, Tex.)
|September 13, 2017
PubMed

Insights

Ionizing radiation (IR) upregulates microRNA-300 (miR-300) in lung cancer cells. Overexpressing miR-300 enhances DNA repair and reduces IR-induced cell cycle arrest and apoptosis by targeting p53 and apaf1.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Radiation Oncology

Background:

  • microRNAs (miRNAs) are key regulators of cellular responses to DNA damage.
  • Previous research implicated miR-300 in cellular responses to chemotherapy and radiation.
  • The specific role and mechanism of miR-300 in DNA damage response in lung cancer remained unclear.

Purpose of the Study:

  • To investigate the role of miR-300 in DNA damage responses induced by ionizing radiation (IR) in human lung cancer.
  • To elucidate the underlying molecular mechanism of miR-300's action in lung cancer cells exposed to IR.

Main Methods:

  • Examined miR-300 expression in lung cancer cells post-IR treatment.
  • Utilized miR-300 mimics for ectopic expression studies.
  • Performed bioinformatic analysis, luciferase reporter assays, Western blotting, flow cytometry, and colony formation assays.

Main Results:

  • IR induced upregulation of endogenous miR-300.
  • Ectopic miR-300 expression enhanced DNA repair and abrogated IR-induced G2 cell cycle arrest and apoptosis.
  • miR-300 directly targeted p53 and apaf1 mRNA, reducing their protein expression.
  • miR-300 overexpression desensitized lung cancer cells to IR by suppressing p53-dependent G2 arrest, apoptosis, and senescence.

Conclusions:

  • miR-300 plays a significant role in regulating cellular sensitivity to ionizing radiation in lung cancer.
  • miR-300 targets p53 and apaf1 to modulate DNA damage responses, cell cycle arrest, apoptosis, and senescence.
  • These findings highlight miR-300 as a potential therapeutic target for enhancing lung cancer treatment efficacy against IR.
Keywords:
apoptosisionizing radiationlung cancermiR-300senescence

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