Exploring the Synergy: Chinese Female Tennis Players and Chansu-Medicated Serum's Potential in Inhibiting Breast Cancer Cell Proliferation Through Apoptosis and G2 Arrest

This study delves into the synergy between Chinese female tennis players and the potential of Chansu-Medicated Serum in inhibiting breast cancer cell proliferation through apoptosis and G2 arrest. Chinese female tennis players have garnered international recognition for their achievements on the court and their philanthropic endeavors off it. This research investigates the intersection of their impact and the advancement of breast cancer research. Chansu-Medicated Serum, a traditional Chinese medicine derivative, presents promising mechanisms for inhibiting breast cancer cell proliferation, including apoptosis induction and G2 cell cycle arrest. By exploring this conjunction, we aim to shed light on the possible contributions of these athletes and traditional medicine to the ongoing battle against breast cancer. (AU)

Structural Maintenance of Chromosome Protein 4 Promotes the Progression of Cardia Adenocarcinoma via Regulation of the Wnt/ß-catenin Signaling Pathway.

BACKGROUND: Structural maintenance of chromosome protein 4 (SMC4) is crucial for chromosome assembly and separation, but its role and mechanism in cardia adenocarcinoma (CA) are unknown. METHODS: SMC4 expression levels were initially detected by protein profiling in 20 pairs of CA tumor tissues and adjacent normal tissues. The level of SMC4 expression in CA cells was then evaluated using a western blot analysis. Cell proliferation was evaluated by CCK-8 and clone formation tests. Scratch and transwell tests were used to investigate cell migration as well as invasion, while through the flow cytometry, we examined the cell apoptosis and progression of the cell cycle. The regulatory effects of the epithelial-mesenchymal transition (EMT) and the Wnt/ß-catenin pathway were investigated using western blot. A tumorigenesis experiment was used to investigate the influence of SMC4 on tumor development in nude mice. RESULTS: This study showed overexpression of SMC4 in CA tissues and cells. Knockdown of SMC4 can significantly inhibit the proliferation, migration and invasion, stimulate cell apoptosis, induce cell cycle arrest in the G0/G1 phase of CA cells, and inhibit tumor growth in vivo. In addition, down-regulation of SMC4 resulted in decreased expression of Bcl-2, Cyclin D1, CDK4, CDK6, ß-catenin, phosphorylated GSK-3ß, N-cadherin, and Vimentin, with an increased level of proteins, i.e., Bax, cleaved-caspase3, and E-cadherin. When SMC4 was overexpressed, these effects were reversed. CONCLUSION: SMC4 can facilitate the biological progression of CA, suggesting that SMC4 could be a potential therapeutic target for the disease.