4.6 Article

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

期刊

MOLECULES
卷 26, 期 16, 页码 -

出版社

MDPI
DOI: 10.3390/molecules26164951

关键词

cervical cancer; short-chain fatty acids; propionic acid; reactive oxygen species; HeLa

资金

  1. Korea Research Institute of Standards and Science [KRISS-2021-GP2021-0003]
  2. Ministry of Science and ICT (MSIT)
  3. National Research Foundation of Korea [NRF-2019M3A9F3065868]
  4. Ministry of Health andWelfare (MOHW)
  5. Korea Health Industry Development Institute (KHIDI) [HI20C0558]
  6. Ministry of Trade, Industry Energy (MOTIE)
  7. Korea Evaluation Institute of Industrial Technology (KEIT) [20009350]
  8. Korea Evaluation Institute of Industrial Technology (KEIT) [20009350] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

Recent studies have shown that propionic acid inhibits the survival of HeLa cells through inducing autophagy, as well as triggering the production of reactive oxygen species (ROS), mitochondrial membrane dysfunction, and affecting the NF-κB and AKT/mTOR signaling pathways.
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-kappa B 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.

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