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JARID1B modulates breast cancer cell apoptosis by regulating p53 expression

Jinghao Wang1, Xiaosong Wu1, Jingxin Wang2

  • 1Department of Pharmacy, The First Affiliated Hospital, Jinan University Guangzhou, China.

International Journal of Clinical and Experimental Pathology
|January 18, 2020
PubMed

Insights

Jumonji AT-rich interactive domain 1B (JARID1B) promotes breast cancer progression. Silencing JARID1B increases apoptosis, partly by modulating p53 expression, suggesting JARID1B as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Jumonji AT-rich interactive domain 1B (JARID1B) is linked to breast cancer progression.
  • The specific role of JARID1B in cancer cell apoptosis remains uninvestigated.

Purpose of the Study:

  • To investigate the impact of JARID1B on breast cancer cell apoptosis.
  • To explore the underlying molecular mechanisms involving p53.

Main Methods:

  • Assessed apoptosis using TUNEL, flow cytometry, and caspase-3 activity.
  • Quantified JARID1B and p53 expression via Western blot.
  • Measured cell viability using MTT assay.
  • Utilized RNA interference (RNAi) and small interfering RNA (siRNA) for gene silencing.

Main Results:

  • JARID1B is overexpressed in breast cancer cell lines and tissues, correlating with poor prognosis.
  • JARID1B silencing significantly enhances breast cancer cell apoptosis.
  • JARID1B modulates p53 expression; its silencing increases p53 protein levels.
  • Inhibition of p53 by siRNA counteracts the pro-apoptotic effect of JARID1B silencing.

Conclusions:

  • JARID1B plays a critical role in regulating breast cancer cell apoptosis.
  • JARID1B may exert its function, in part, through the p53 pathway.
  • Targeting JARID1B could represent a novel therapeutic strategy for breast cancer.
Keywords:
Breast cancerJARID1Bapoptosisp53

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