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Effect of Rab23 on the proliferation and apoptosis in breast cancer

Yali Liu1, Chao Zeng1, Nandi Bao2

  • 1Department of Physiology, State Key Discipline of Cell Biology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.

Oncology Reports
|August 5, 2015
PubMed

Insights

Rab23 is expressed in breast cancer cells and inhibits their growth and proliferation. Overexpression of Rab23 induces apoptosis, suggesting it

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The Hedgehog (Hh) signaling pathway plays a crucial role in various cancers.
  • Rab23 acts as a negative regulator of the Hh pathway.
  • Dysregulation of Hh signaling is implicated in carcinoma development.

Purpose of the Study:

  • To investigate Rab23 expression in breast cancer cell lines.
  • To determine the effect of Rab23 on breast cancer cell viability and proliferation.
  • To elucidate the mechanism by which Rab23 regulates the Hh pathway in breast cancer.

Main Methods:

  • Rab23 expression analyzed by RT-PCR, western blotting, and immunofluorescence.
  • Cell viability and proliferation assessed using MTT, colony formation, and BrdU assays.
  • Cell cycle distribution and apoptosis evaluated by flow cytometry (FCM).
  • Hedgehog pathway regulation studied by detecting Gli molecule levels via RT-PCR.

Main Results:

  • Rab23 mRNA and protein are expressed in breast cancer cells (MDA-MB-231, Bcap37, MCF-7).
  • Rab23 overexpression reduced cell viability, colony formation, and BrdU incorporation.
  • Rab23 induced G1 cell cycle arrest, decreased S phase population, and promoted apoptosis.
  • Rab23 decreased Gli1 and Gli2 mRNA levels, indicating Hh pathway inhibition.

Conclusions:

  • Rab23 is expressed in breast cancer cells and inhibits their growth and proliferation.
  • Rab23 induces apoptosis in breast cancer cells, potentially via Gli1 and Gli2 downregulation.
  • Rab23 represents a potential therapeutic target for breast cancer treatment.

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