2. Academic Validation
  3. Preliminary investigation on the mechanism of baicalein regulating the effects of Nischarin on invasion and apoptosis of human breast cancer cells MCF-7 through Wnt3α/β-catenin pathway

Preliminary investigation on the mechanism of baicalein regulating the effects of Nischarin on invasion and apoptosis of human breast cancer cells MCF-7 through Wnt3α/β-catenin pathway

  • Int Immunopharmacol. 2024 Dec 25;143(Pt 1):113262. doi: 10.1016/j.intimp.2024.113262.
Gaojian He 1,  Xuemei Huang 2,  Yun Dong 3,  Kun Chen 4,  Xuefeng He 4,  Meitong Pan 4,  Weicheng Zeng 5,  Xiaolan Yu 6,  Jiyi Xia 7
Affiliations

Affiliations

  • 1 Dean's Office, Dazhou Vocational College of Chinese Medicine, Dazhou, China.
  • 2 Department of Oncology and Hematology, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
  • 3 Department of Traditional Chinese Medicine, Dazhou Vocational College of Chinese Medicine, Dazhou, China.
  • 4 Department of Technology and Social Services,Dazhou Vocational College of Chinese Medicine, Dazhou, China.
  • 5 College of Integration of Traditional Chinese And Western Medicine, Southwest Medical University, Luzhou, China.
  • 6 Department of Obstetrics and Gynecology, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, China. Electronic address: yuxiaolan129@yeah.net.
  • 7 Department of Technology and Social Services,Dazhou Vocational College of Chinese Medicine, Dazhou, China; Dazhou Chinese Medicine Research and Development Center, Dazhou, China. Electronic address: yuxiaolan-xiajiyi@swmu.edu.cn.
PMID: 39353394 DOI: 10.1016/j.intimp.2024.113262
Abstract

Background: Breast Cancer (BC) remains the leading cause of cancer-related mortality in women. Here, we investigate the anti-tumor effects of baicalein on human BC cells (MCF-7 cells) and explore if it regulates the Nischarin protein via Wnt3α/β-catenin signaling pathway.

Methods: We employed Wnt3α and DKK-1 to activate and inhibit the Wnt/β-catenin signaling pathway, respectively. We used CCK-8 cell viability, flow cytometry Apoptosis, wound-healing and transwell migration/invasion assays. Further, using western blotting and real-time quantitative PCR (q-PCR) we analyzed expression levels of Nischarin, MMP-9, Wnt/β-catenin pathway (β-catenin, Axin 1), and apoptotic pathway (Bax, Bcl-2) proteins and their mRNAs.

Results: We found that baicalein inhibits MCF-7 cell viability and promotes Apoptosis (evidenced by increased Bax and decreased Bcl-2 expressions) in a concentration-dependent manner. It also inhibits TPA-induced migration and invasion, and downregulates MMP-9 expression. Baicalein reverses the increase in cell viability caused by Wnt3α-induced Wnt/β-catenin pathway activation. Conversely, baicalein counteracts the increase in Apoptosis caused by DKK-1 mediated inhibition of the Wnt/β-catenin pathway. Additionally, baicalein upregulates Nischarin expression via modulating the Wnt/β-catenin pathway as indicated by the antagonistic effects of Wnt3α and DKK-1 on this effect of baicalein.

Conclusion: Baicalein exerts anti-tumor effects on MCF-7 cells through the Wnt3α/β-catenin signaling pathway, and promotes Apoptosis and inhibits migration and invasion. The upregulation of Nischarin by baicalein further suggests a potential therapeutic target for BC treatment.

Keywords

Apoptosis; Baicalein; Invasion; Migration; Nischarin; TPA; Wnt3α/β-catenin signaling.

Figures
Products