Polyphyllin VII inhibits triple-negative breast cancer via THOP1 modulation

Authors

  • Xueyan Fu Department of Breast Surgery, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou Hospital of Traditional Chinese Medicine, 310007 Hangzhou, Zhejiang, China Author
  • Wangjin Xu Department of Breast Surgery, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou Hospital of Traditional Chinese Medicine, 310007 Hangzhou, Zhejiang, China Author
  • Tian Lan Department of Breast Surgery, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou Hospital of Traditional Chinese Medicine, 310007 Hangzhou, Zhejiang, China Author

DOI:

https://doi.org/10.62767/

Keywords:

polyphyllin VII, TNBC, apoptosis, THOP1

Abstract

Objective: We assessed the role of polyphyllin VII in triple-negative breast cancer (TNBC) and investigated the potential molecular mechanism. Methods: Cellular proliferation was measured using the CCK-8 assay. To evaluate colony formation and cell migration, we conducted colony formation assays and transwell analyses. Apoptotic protein levels were determined through Western blot. The in vivo anti-TNBC efficacy of polyphyllin VII were evaluated using xenograft tumor models. Results: Polyphyllin VII exhibited inhibitory effects on cellular proliferation, colony formation, migration, and also induced apoptosis. Polyphyllin VII downregulated THOP1 expression in TNBC. THOP1 overexpression noticeably reversed the aforementioned effects of polyphyllin VII. In vivo, polyphyllin VII demonstrated inhibition of TNBC tumor growth and THOP1 expression, while simultaneously upregulating cleaved caspase 3. Conclusion: These results demonstrated that polyphyllin VII induced apoptosis by regulating THOP1 in TNBC. THOP1 is therefore proposed as a potential novel target of polyphyllin VII for combating TNBC.

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Published

2026-09-30

Data Availability Statement

The data presented in this study are available on request from the corresponding author.

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Section

Original Research

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