Natural compound catechol induces DNA damage, apoptosis, and G1 cell cycle arrest in breast cancer cells

Cijo George Vazhappilly1, Rawad Hodeify1, Shoib Sarwar Siddiqui1

  • 1Department of Biotechnology, American University of Ras Al Khaimah, Ras Al Khaimah, United Arab Emirates.

Insights

Catechol, a plant compound, effectively inhibits breast cancer cell growth and proliferation by inducing DNA damage and activating cell death pathways. It shows a favorable safety profile, sparing noncancerous cells while targeting cancer cells specifically.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Targeting cell cycle and DNA damage pathways are key strategies for breast cancer therapy.
  • Natural small molecules show promise against resistant and aggressive breast cancers.

Purpose of the Study:

  • To investigate the chemotherapeutic efficacy and specificity of catechol in breast cancer cells.
  • To elucidate the mechanisms underlying catechol's anti-cancer effects.

Main Methods:

  • Assessing catechol's cytotoxicity and antiproliferative effects on MCF-7 and MDA-MB-231 breast cancer cells and noncancerous cells.
  • Analyzing DNA damage response via ATM/ATR pathways and γ-H2AX expression.
  • Investigating cell cycle arrest (G1 phase) and apoptosis induction through p53, caspase activation, and key protein regulation (p21, DNMT1, p-BRCA1, MCL-1, PDCD6, Bax/Bcl-2).

Main Results:

  • Catechol demonstrated concentration-dependent cytotoxicity and antiproliferative effects on breast cancer cells, with minimal impact on noncancerous cells.
  • Catechol induced DNA double-strand breaks via ATM/ATR activation and enhanced γ-H2AX expression.
  • Catechol caused G1 cell cycle arrest in MCF-7 cells and triggered apoptosis by modulating p53, caspase pathways, and key regulatory proteins, leading to an increased Bax/Bcl-2 ratio.

Conclusions:

  • Catechol exhibits a favorable safety profile against noncancerous cells.
  • Catechol effectively targets multiple signaling cascades to inhibit breast cancer cell proliferation and induce cell death.

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