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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...

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Related Experiment Video

Updated: Dec 10, 2025

Proton Therapy Delivery and Its Clinical Application in Select Solid Tumor Malignancies

Proton Therapy Delivery and Its Clinical Application in Select Solid Tumor Malignancies

Published on: February 6, 2019

PP2A and tumor radiotherapy.

Xiao Lei¹, Na Ma¹, Lehui Du¹

¹The First Medical Center of Chinese PLA General Hospital, Department of Radiation Oncology, Beijing, P. R. China.

|August 28, 2020

Summary

This summary is machine-generated.

Inhibiting Protein Phosphatase 2A (PP2A) in cancer cells can enhance their sensitivity to chemoradiotherapy. This approach disrupts mitosis, making tumor cells more susceptible to cell death and slowing cancer growth.

Keywords:

Conventional tumor radiotherapy DNA damage response Protein phosphatase 2A Radiosensitization effects

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Published on: May 9, 2025

Area of Science:

Molecular Biology
Oncology
Cellular Physiology

Background:

Protein Phosphatase 2A (PP2A) is a crucial serine/threonine phosphatase regulating apoptosis, mitosis, and DNA damage responses.
PP2A traditionally functions as a tumor suppressor, but its inhibition is emerging as a therapeutic strategy.

Purpose of the Study:

To review the current understanding of PP2A's role in tumor radiotherapy.
To explore potential mechanisms by which PP2A inhibition influences radiotherapy efficacy.

Main Methods:

Literature review of studies on PP2A, cancer, and radiotherapy.
Analysis of cellular and molecular mechanisms linking PP2A activity to treatment response.

Main Results:

PP2A inhibition can induce mitotic catastrophe in tumor cells, increasing radiosensitivity.
Evidence suggests PP2A inhibition slows tumor growth across various cancer types post-radiotherapy.

Conclusions:

Targeting PP2A activity represents a promising strategy to enhance chemoradiotherapy outcomes.
Further research into PP2A's mechanisms in cancer treatment is warranted.