2. Academic Validation
  3. Formosanin C inhibits triple-negative breast cancer progression by suppressing the phosphorylation of STAT3 and the polarization of M2 macrophages

Formosanin C inhibits triple-negative breast cancer progression by suppressing the phosphorylation of STAT3 and the polarization of M2 macrophages

  • Breast Cancer Res Treat. 2025 May;211(1):71-89. doi: 10.1007/s10549-025-07623-8.
Yin-Wei Dai # 1 2,  Zhi-Xuan Wu # 1,  Yao Cheng # 1,  Hao-Dong Wu 1,  Jia-Wei Chen 3,  Lin-Xi Lv 1 4,  Zi-Qiong Wang 1,  Hong-Feng Li 1,  Cong-Zhi Yan 1,  Jing-Xia Bao 1,  Cong-Hui Liu 1,  Xuan-Xuan Dai 5 6
Affiliations

Affiliations

  • 1 Department of Breast Surgery, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 2 Department of Obstetrics and Gynecology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
  • 3 Department of Hepatopancreatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 4 Wenzhou Medical University, Wenzhou, Zhejiang, China.
  • 5 Department of Breast Surgery, Key Laboratory of Clinical Laboratory Diagnosis and Translational Research of Zhejiang Province, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China. daoshidaixuanxuan@126.com.
  • 6 Zhejiang Key Laboratory of Intelligent Cancer Biomarker Discovery and Translation, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. daoshidaixuanxuan@126.com.
  • # Contributed equally.
PMID: 39953272 DOI: 10.1007/s10549-025-07623-8
Abstract

Introduction: Triple-negative breast Cancer (TNBC), is a highly aggressive tumor. Formosanin C (FC) is a diosgenin with immunomodulatory and antitumor properties, the precise mechanism through which it is against TNBC remains uncertain.

Objective: Clarifying the mechanism of FC against TNBC.

Materials and methods: The impact of FC on two TNBC cell lines for 24 h was investigated through various techniques including the CCK8 assay, flow cytometry, transwell assay, scratch tests, immunoblot assay, and immunofluorescence. To elucidate the mechanism behind the anti-TNBC effect of FC, MDA-MB-231 cells were subjected to STAT3 overexpression. Moreover, the in vivo efficacy of FC was examined using a xenograft nude mice (BALB/C). Mice were divided into the control group (equal amount of PBS), the napabucasin group (5 mg/kg) and the FC groups (1 mg/kg, 2 mg/kg). The study duration was 30 days.

Results: FC exhibited inhibitory effects against MDA-MB-231 and Hs578T cells. FC can decrease the migratory capacity of TNBC cells by inhibiting epithelial-mesenchymal transition (EMT). Meanwhile, we demonstrated that the inhibition of phosphorylation of STAT3 (Y705) is the crucial mechanism of FC against TNBC. Moreover, FC also hindered the polarization of macrophage M2.

Discussion and conclusion: This study is the first to show that FC restrains the EMT of TNBC cells by obstructing the STAT3 pathway and hinders the M2 polarization of macrophages and immune evasion. Therefore, FC holds the possibility of being utilized as a therapeutic remedy for TNBC.

Keywords

Epithelial-mesenchymal transition; Network pharmacology; Single-cell sequencing.

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