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miR-3188 Enhances Sensitivity of Breast Cancer Cells to Ionizing Radiation by Down-regulating Rictor

Sung-Eun Hong1, Hyeon-Ok Jin1, Seung-Mi Kim1

  • 1KIRAMS Radiation Biobank, Korea Institute of Radiological and Medical Sciences, Seoul, Republic of Korea.

Anticancer Research
|December 1, 2021
PubMed
Abstract

Insights

MicroRNA-3188 targets Rictor, inhibiting breast cancer cell growth and enhancing radiation sensitivity. This suggests miR-3188 as a potential therapeutic agent for breast cancer treatment.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Rictor protein is crucial for mTORC2 complex formation, regulating cell growth and survival.
  • Dysregulation of Rictor and mTORC2 signaling is implicated in breast cancer progression.

Purpose of the Study:

  • To identify microRNAs (miRNAs) that target and down-regulate Rictor.
  • To investigate the functional impact of these miRNAs on breast cancer cell survival and response to therapy.

Main Methods:

  • Utilized breast cancer cell lines (HCC1954, MDA-MB-231, SK-BR-3, BT474).
  • Employed trypan blue and MTT assays for cell viability.
  • Performed PCR, luciferase reporter assays, and Western blotting to assess gene and protein expression.
  • Investigated the effect of miRNA overexpression on ionizing radiation (IR) sensitivity.

Main Results:

  • Overexpression of miR-3188 significantly suppressed Rictor expression and reduced cell viability in HCC1954 and MDA-MB-231 cells.
  • miR-3188 reduced phosphorylation of AKT at Ser473, a key downstream target of mTORC2.
  • miR-3188 overexpression sensitized breast cancer cells to ionizing radiation by down-regulating Rictor and p-AKT.

Conclusions:

  • miR-3188 enhances ionizing radiation sensitivity in breast cancer by targeting Rictor and impacting the mTORC2/AKT pathway.
  • Modulating miR-3188 offers a potential therapeutic strategy for improving breast cancer treatment outcomes.
Keywords:
Breast cancerRictorionizing radiationmiR-3188

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