2. Academic Validation
  3. Notoginsenoside Ft1 inhibits colorectal cancer growth by increasing CD8+ T cell proportion in tumor-bearing mice through the USP9X signaling pathway

Notoginsenoside Ft1 inhibits colorectal cancer growth by increasing CD8+ T cell proportion in tumor-bearing mice through the USP9X signaling pathway

  • Chin J Nat Med. 2024 Apr;22(4):329-340. doi: 10.1016/S1875-5364(24)60623-0.
Yutao Feng 1,  Yuan Li 1,  Fen Ma 1,  Enjiang Wu 1,  Zewei Cheng 1,  Shiling Zhou 1,  Zhengtao Wang 1,  Li Yang 2,  Xun Sun 3,  Jiwei Zhang 4
Affiliations

Affiliations

  • 1 Shanghai Key Laboratory of Compound Chinese Medicines, The MOE Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
  • 2 Shanghai Key Laboratory of Compound Chinese Medicines, The MOE Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address: yl7@shutcm.edu.cn.
  • 3 Gastrointestinal surgery, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China. Electronic address: shsunxun@sina.cn.
  • 4 Shanghai Key Laboratory of Compound Chinese Medicines, The MOE Key Laboratory for Standardization of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China. Electronic address: joezhang@shutcm.edu.cn.
PMID: 38658096 DOI: 10.1016/S1875-5364(24)60623-0
Abstract

The management of colorectal Cancer (CRC) poses a significant challenge, necessitating the development of innovative and effective therapeutics. Our research has shown that notoginsenoside Ft1 (Ng-Ft1), a small molecule, markedly inhibits subcutaneous tumor formation in CRC and enhances the proportion of CD8+ T cells in tumor-bearing mice, thus restraining tumor growth. Investigation into the mechanism revealed that Ng-Ft1 selectively targets the deubiquitination enzyme USP9X, undermining its role in shielding β-catenin. This leads to a reduction in the expression of downstream effectors in the Wnt signaling pathway. These findings indicate that Ng-Ft1 could be a promising small-molecule treatment for CRC, working by blocking tumor progression via the Wnt signaling pathway and augmenting CD8+ T cell prevalence within the tumor environment.

Keywords

CD8(+) T cell; Colorectal cancer; Notoginsenoside Ft1; Ubiquitin-specific peptidase 9 X-linked; Wnt; β-Catenin.

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