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Triptonide Inhibits the Cervical Cancer Cell Growth via Downregulating the RTKs and Inactivating the Akt-mTOR Pathway

Li-Na Zhou1,2, Shi-Qing Peng2, Xue-Lian Chen3

  • 1Department of Radiotherapy & Oncology, The Second Affiliated Hospital of Soochow University, Institute of Radiation Oncology, Soochow University, 215004 Suzhou, China.

Oxidative Medicine and Cellular Longevity
|September 16, 2024
PubMed

Insights

Triptonide (TN), derived from a Chinese herb, effectively inhibits cervical cancer growth and invasion by targeting key signaling pathways. This novel therapeutic shows promise for treating cervical cancer with minimal toxicity to normal cells.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Cervical cancer (CC) presents a significant global health challenge with high incidence and mortality rates.
  • Novel therapeutic strategies are urgently needed to combat this disease.
  • Triptonide (TN) is a promising small molecule derived from the Chinese herb *Tripterygium wilfordii Hook*.

Purpose of the Study:

  • To investigate the anti-cancer effects of Triptonide (TN) on human cervical cancer cells both *in vitro* and *in vivo*.
  • To elucidate the molecular mechanisms underlying TN's therapeutic activity.
  • To assess the safety profile of TN on normal cervical epithelial and fibroblast cells.

Main Methods:

  • Cell viability, proliferation, colony formation, migration, and invasion assays were performed on human cervical cancer cells treated with TN.
  • Apoptosis and cell cycle analysis were conducted.
  • RNA sequencing and Gene Set Enrichment Analysis (GSEA) were employed to identify differentially expressed genes and enriched pathways.
  • Western blotting was used to assess protein expression and pathway activation.
  • *In vivo* studies involved subcutaneous xenograft models in nude mice treated with oral TN.

Main Results:

  • TN significantly inhibited cervical cancer cell growth, proliferation, migration, and invasion at nanomolar concentrations.
  • TN induced apoptosis and cell cycle arrest in cancer cells while sparing normal cells.
  • GSEA revealed enrichment in receptor tyrosine kinase (RTK) signaling and the PI3K-Akt-mTOR pathway.
  • TN treatment led to downregulation of EGFR and PDGFRα and inhibition of Akt-mTOR activation.
  • *In vivo*, oral TN administration suppressed tumor growth in xenograft models, consistent with *in vitro* findings.

Conclusions:

  • Triptonide (TN) exhibits potent anti-cancer activity against cervical cancer cells *in vitro* and *in vivo*.
  • TN's therapeutic effects are associated with the downregulation of RTKs (EGFR, PDGFRα) and inactivation of the Akt-mTOR signaling pathway.
  • TN represents a potential novel therapeutic agent for cervical cancer treatment.

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