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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 daughter...

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Related Experiment Video

Updated: Jun 7, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Curcumin-altered p53-response genes regulate radiosensitivity in p53-mutant Ewing's sarcoma cells.

J Veeraraghavan¹, M Natarajan, T S Herman

¹Department of Radiation Oncology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.

Anticancer Research

|November 2, 2010

Summary

Curcumin enhances radiation therapy in p53 mutant Ewing sarcoma cells by affecting apoptosis and DNA damage. This suggests curcumin as a potential radiosensitizer, though its p53-independent effects require further study.

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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

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Published on: December 30, 2025

Area of Science:

Oncology
Molecular Biology
Radiotherapy

Background:

Curcumin exhibits antitumor properties, including radiosensitization, by targeting molecules like p53.
Ewing's sarcoma (ES) is a cancer often characterized by p53 mutations.

Purpose of the Study:

To investigate the radiosensitizing effect of curcumin in p53-mutant Ewing's sarcoma (ES) cells.
To explore curcumin's impact on p53 downstream targets and related cellular processes.

Main Methods:

ES cells were treated with radiation and/or curcumin.
Transcriptional and translational levels of p53 downstream targets were analyzed.
Apoptosis, DNA fragmentation, cell survival, and clonal expansion were assessed.

Main Results:

Curcumin modulated the expression of p21, Bax, BclXl, and Mcl1 in response to radiation.
Radiation with or without curcumin did not alter p53 levels.
Curcumin enhanced radiation-induced apoptosis, DNA fragmentation, cytotoxicity, and clonal expansion.

Conclusions:

Curcumin demonstrates radiosensitizing potential in p53-mutant ES cells.
The radiosensitization appears to be mediated through the regulation of IR-modulated p53-response genes.
Further research is needed to understand the p53-independent mechanisms of curcumin's action.