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Updated: Nov 6, 2025

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CIP2A silencing alleviates doxorubicin resistance in MCF7/ADR cells through activating PP2A and autophagy

Z Zhu1, Z Wei2

  • 1Department of Radiotherapy, Cangzhou Central Hospital, No.16 Xinhua West Rd, Cangzhou city, Hebei Province, 061000, China. zhuzhongcheng066@163.com.

Clinical & Translational Oncology : Official Publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
|May 5, 2021
PubMed
Abstract

Insights

Silencing cancerous inhibitor of protein phosphatase 2A (CIP2A) enhances doxorubicin treatment effects in breast cancer cells. This approach increases apoptosis and reduces proliferation and migration, offering potential for overcoming doxorubicin resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cancerous inhibitor of protein phosphatase 2A (CIP2A) is implicated in various cancer pathologies.
  • Doxorubicin resistance is a significant challenge in breast cancer treatment.

Purpose of the Study:

  • To investigate if modulating CIP2A levels can improve doxorubicin efficacy in MCF-7/ADR cells.
  • To explore the mechanisms underlying CIP2A's role in doxorubicin resistance.

Main Methods:

  • CIP2A was silenced using small interfering RNAs (siRNAs).
  • Cell proliferation was assessed via MTT assay.
  • Cell migration was evaluated using wound healing assays, and apoptosis was measured by caspase-3/-7 activity.

Main Results:

  • Doxorubicin suppressed MCF-7/ADR cell proliferation dose-dependently.
  • CIP2A knockdown further reduced cell proliferation and migration, even with doxorubicin treatment.
  • CIP2A silencing enhanced apoptosis, increased phosphatase 2A (PP2A) activity, and upregulated autophagy markers LC3B and Beclin1.

Conclusions:

  • Targeting CIP2A holds promise for enhancing chemotherapy effectiveness.
  • CIP2A inhibition may represent a viable strategy to overcome doxorubicin resistance in breast cancer.
Keywords:
AutophagyCIP2ADoxorubicinMCF7 cellPP2A

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