Nitidine Chloride Triggers Autophagy and Apoptosis of Ovarian Cancer Cells through Akt/mTOR Signaling Pathway

Curr Pharm Des. 2023;29(19):1524-1534. doi: 10.2174/1381612829666230614154847.

Abstract

Objective: Ovarian cancer (OC) is the eighth most common cancer with high mortality in women worldwide. Currently, compounds derived from Chinese herbal medicine have provided a new angle for OC treatment.

Methods: In this study, the cell proliferation and migration of ovarian cancer A2780/SKOV3 cells were inhibited after being treated with nitidine chloride (NC) by using MTT and Wound-Healing Assay. Flow cytometry analysis indicated NC-induced apoptosis of ovarian cancer cells, and AO and MDC staining showed that NC treatment induced the appearance of autophagosomes and autophagic lysosomes in ovarian cancer cells.

Results: Through the autophagy inhibition experiment of chloroquine, it was proved that NC significantly further promoted apoptosis in ovarian cancer cells. Furthermore, NC proved that it could significantly decrease the expression of autophagy-related genes such as Akt, mTOR, P85 S6K, P70 S6K, and 4E-BP1.

Conclusion: Therefore, we suggest that NC could trigger autophagy and apoptosis of ovarian cancer cells through Akt/mTOR signaling pathway, and NC may potentially be a target for chemotherapy against ovarian cancer.

Keywords: Akt/mTOR pathway; Ovarian cancer; cell apoptosis; cell autophagy; cell proliferation; nitidine chloride.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Autophagy / physiology
  • Cell Line, Tumor
  • Cell Proliferation
  • Female
  • Humans
  • Ovarian Neoplasms* / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases

Substances

  • Proto-Oncogene Proteins c-akt
  • nitidine
  • TOR Serine-Threonine Kinases