[Effects of CSN4 knockdown on proliferation and apoptosis of breast cancer MDA-MB-231 cells].

Breast cancer is one of the most common malignant tumors endangering women. It has been found that the subunits of the COP9 complex are closely related to the occurrence and development of malignant tumors, and the CSN4 subunit plays an important role in regulating the whole complex. In the breast cancer cell line MDA-MB-231, we successfully established a lentivirus-mediated CSN4-knockdown cell line. CCK8 cell proliferation assays and colony formation experiments confirmed that CSN4 knockdown significantly decreased the cellular proliferation rate. Cell cycle analysis showed that CSN4 knockdown increased sub-G1 population and induced apoptosis. In addition, Western blotting assays confirmed that CSN4 regulates the expression of CDK6 and Caspase3, suggesting that CSN4 modulates the proliferation and apoptosis of breast cancer cells by regulating the expression of CDK6 and Caspase3 genes and thereby tumorigenesis. This study has deepened our understanding of the molecular mechanism of apoptosis and cell growth in breast cancers, and further revealed the role and mechanism of CSN4 in cancer biology.

Effects of Shugan Jianpi Formula () on myeloid-derived suppression cells-mediated depression breast cancer mice / 中国结合医学杂志

<p><b>OBJECTIVE</b>To observe the intervention effect of Shugan Jianpi Formula (, SGJPF) on a breast cancer mouse model with depression and investigate the underlying mechanism of SGJPF in preventing the development of breast cancer.</p><p><b>METHODS</b>The breast cancer model was induced by inoculation of breast cancer cells, the depression model was induced by chronic stress stimuli, and the depression cancer model was established by combining the two factors. The mice were divided into 7 groups: normal control, depression model, tumor model, depression tumor model, SGJPF, chemotherapy, and SGJPF+chemotherapy groups. The last 3 groups were depression breast cancer mice and treated respectively with SGJPF, chemotherapy drug gemcitabine (GEM), and SGJPF alongside GEM. The condition of the mice was evaluated by the expression of 5-hydroxytryptamine in hippocampus after the sucrose water test and open field test, weight change, and survival time. Tumor growth was monitored with in vivo imaging. Flow cytometry was used to analyze the level of myeloid-derived suppression cell (MDSC) in the mouse spleen, T cell subsets, and the early apoptosis of CD8T cells.</p><p><b>RESULTS</b>The SGJPF+GEM group had the highest inhibition rate and the longest survival time (P<0.01). The MDSC level and the apoptosis rate of CD8T cells was the highest in the SGJPF+GEM group (P<0.05).</p><p><b>CONCLUSIONS</b>Depressive disorders and tumor growth could suppress the immune function of mice to different degrees, and the microenvironment in late 4T1 inflammatory breast cancer may play an important role in the pathological process. SGJYF could regulate the immune microenvironment by reducing CD8T lymphocyte apoptosis and tumor cell activity, increasing immune surveillance capability, and inhibiting MDSC proliferation, thus prolonging the survival time of tumor-bearing mice.</p>