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Anticancer Effects of Propionic Acid Inducing Cell Death in Cervical Cancer Cells.

Abstract
Recent studies found that short-chain fatty acids (SCFAs), which are produced through bacterial fermentation in the gastrointestinal tract, have oncoprotective effects against cervical cancer. The most common SCFAs that are well known include acetic acid, butyric acid, and propionic acid, among which propionic acid (PA) has been reported to induce apoptosis in HeLa cells. However, the mechanism in which SCFAs suppress HeLa cell viability remain poorly understood. Our study aims to provide a more detailed look into the mechanism of PA in HeLa cells. Flow cytometry analysis revealed that PA induces reactive oxygen species (ROS), leading to the dysfunction of the mitochondrial membrane. Moreover, PA inhibits NF-κB and AKT/mTOR signaling pathways and induces LC3B protein levels, resulting in autophagy. PA also increased the sub-G1 cell population that is characteristic of cell death. Therefore, the results of this study propose that PA inhibits HeLa cell viability through a mechanism mediated by the induction of autophagy. The study also suggests a new approach for cervical cancer therapeutics.
AuthorsChau Ha Pham, Joo-Eun Lee, Jinha Yu, Sung Hoon Lee, Kyung-Rok Yu, Jaewoo Hong, Namki Cho, Seil Kim, Dukjin Kang, Soojin Lee, Hee Min Yoo
JournalMolecules (Basel, Switzerland) (Molecules) Vol. 26 Issue 16 (Aug 16 2021) ISSN: 1420-3049 [Electronic] Switzerland
PMID34443546 (Publication Type: Journal Article)
Chemical References
  • Antineoplastic Agents
  • NF-kappa B
  • Propionates
  • Reactive Oxygen Species
  • propionic acid
Topics
  • Antineoplastic Agents (chemistry, pharmacology)
  • Autophagy (drug effects)
  • Cell Cycle (drug effects)
  • Cell Death (drug effects)
  • Female
  • HeLa Cells
  • Humans
  • Mitochondrial Membranes (drug effects, metabolism)
  • NF-kappa B (metabolism)
  • Propionates (chemistry, pharmacology)
  • Reactive Oxygen Species (metabolism)
  • Signal Transduction (drug effects)
  • Uterine Cervical Neoplasms (metabolism, pathology)

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