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

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

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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.

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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.