4.6 Article

Gallic Acid Induces S and G2 Phase Arrest and Apoptosis in Human Ovarian Cancer Cells In Vitro

Journal

APPLIED SCIENCES-BASEL
Volume 11, Issue 9, Pages -

Publisher

MDPI
DOI: 10.3390/app11093807

Keywords

ovarian cancer; apoptosis; gallic acid; cell cycle arrest

Funding

  1. NIH from the National Center for Research Resources [P20RR016477]
  2. NIH from National Center for Research Resources (NIGMS) [P20GM103434]
  3. key research and development program of Zhejiang Province [2020C02040, 2020C02019]
  4. People's Government of Zhejiang Province [2019SY03]
  5. Natural Science Foundation of Xinjiang Uygur Autonomous Region [2021D01A71]
  6. Public Projects of Zhejiang Province [LGC19C200008]
  7. NIGMS, a component of the National Institutes of Health (NIH) [P20GM104932]
  8. COBRE [GM102488/RR032138]
  9. ARIA S10 grant [RR020866]
  10. FORTESSA S10 grant [OD016165]
  11. Tumor Microenvironment (TME) CoBRE Grant [NIH/NIGMS P20GM121322]
  12. West Virginia IDeA-CTR [NIH/NIGMS 2U54 GM104942-03]
  13. National Science Foundation [NSF/1920920, NSF/1761792]
  14. Chinese Academy of Forestry [2019SY03]

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The study demonstrated that gallic acid (GA) can inhibit ovarian cancer cell proliferation by promoting apoptosis and blocking cell cycle progression, indicating its potential preventive and therapeutic effects in ovarian cancer.
Ovarian cancer (OC) is among the top gynecologic cancers in the US with a death tally of 13,940 in the past year alone. Gallic acid (GA) is a natural compound with pharmacological benefits. In this research, the role of GA on cell proliferation, cell apoptosis, cell cycle-related protein expression was explored in OC cell lines OVCAR-3 and A2780/CP70. After 24, 48 and 72 h of GA treatment, the IC50 values in OVCAR-3 cells were 22.14 +/- 0.45, 20.36 +/- 0.18, 15.13 +/- 0.53 mu M, respectively and in A2780/CP70 cells IC50 values were 33.53 +/- 2.64, 27.18 +/- 0.22, 22.81 +/- 0.56, respectively. Hoechst 33,342 DNA staining and flow cytometry results showed 20 mu M GA exposure could significantly accelerate apoptosis in both OC cell lines and the total apoptotic rate increased from 5.34%(control) to 21.42% in OVCAR-3 cells and from 8.01%(control) to 17.69% in A2780/CP70 cells. Western blot analysis revealed that GA stimulated programmed OC cell death via a p53-dependent intrinsic signaling. In addition, GA arrested cell cycle at the S or G2 phase via p53-p21-Cdc2-cyclin B pathway in the same cells. In conclusion, we provide some evidence of the efficacy of GA in ovarian cancer prevention and therapy.

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