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Updated: Jan 15, 2026

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

Published on: December 30, 2025

22

p53 mediates the cellular responses to cis-trimethoxystilbene in breast cancer cell lines

Julia Mirian Paulino1, Natália Dos Santos Gonçalves1, Heber Eduardo Andrada1

  • 1Laboratory of Genetics and Molecular Biology, University of Franca, Franca, SP, Brazil.

Natural Product Research
|October 7, 2025
PubMed

Insights

The compound cis-trimethoxystilbene (cis-TMS) effectively inhibits chemoresistant breast cancer cell growth and induces apoptosis. Its efficacy is dependent on the p53 tumor suppressor protein, suggesting a targeted therapy approach.

Area of Science:

  • * Molecular Biology
  • * Cancer Research
  • * Pharmacology

Background:

  • * Chemotherapy resistance in breast cancer presents a significant clinical challenge.
  • * The tumor suppressor protein p53 plays a critical role in cellular responses to DNA damage and stress.
  • * Novel therapeutic agents targeting cancer-specific pathways are needed.

Purpose of the Study:

  • * To investigate the anti-cancer effects of cis-trimethoxystilbene (cis-TMS) on chemoresistant breast cancer cells.
  • * To elucidate the role of the p53 protein in mediating cis-TMS-induced cellular responses.
  • * To explore cis-TMS as a potential targeted therapy for breast cancer.

Main Methods:

  • * Cell viability assays were performed on MDA-MB-231 breast cancer cells treated with cis-TMS.
  • * Apoptosis rates were quantified using flow cytometry.
  • * p53 gene silencing was employed in MCF-10A and MCF-7 cell lines to assess p53 dependency.
  • * Protein interaction studies were conducted to evaluate cis-TMS binding with p53.

Main Results:

  • * cis-TMS significantly inhibited MDA-MB-231 cell growth, reducing viability by ~75% at 2.5 µM.
  • * cis-TMS treatment increased apoptosis rates in cancer cells by nearly 20%.
  • * cis-TMS-induced apoptosis and cell cycle arrest were found to be p53-dependent.
  • * cis-TMS did not alter p53 conformation at low concentrations but may affect its activity at higher doses.

Conclusions:

  • * cis-TMS demonstrates potent anti-cancer activity against chemoresistant breast cancer cells.
  • * The therapeutic efficacy of cis-TMS is critically dependent on functional p53.
  • * cis-TMS selectively targets cancer cells with functional p53, indicating potential for targeted therapy.
  • * Further research is required to optimize cis-TMS therapeutic strategies, considering p53 reliance and potential genomic instability risks.
Keywords:
Cis-trimethoxystilbeneDNA damagebreast cancerp53

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