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Breast cancer is the most common malignant tumor in women and the main cancer causing death in females. Breast cancer therefore seriously threatens women's health and life span. Although there are a variety of comprehensive and multidisciplinary treatments for different types of breast cancer, the overall prognosis of advanced breast cancer remains unsatisfactory. The incidence of breast cancer is increasing year by year, and the age of onset is gradually decreasing, making the discovery of a breakthrough in breast cancer treatment a major problem that needs to be solved urgently. A large number of studies have shown the growth of breast cancer cells can be inhibited by inducing ferroptosis. Acid sphingomyelinase has also been confirmed to be involved in cell death induced by ferroptotic agonists. This article reviews the progress in the use of acid sphingomyelinase and ferroptosis in the treatment of breast cancer, and summarizes the mechanism of ferroptosis in breast cancer cells and its correlation with acid sphingomyelinase. This review will provide a theoretical foundation for seeking new therapeutic targets for breast cancer. [ABSTRACT FROM AUTHOR]

Background and purpose: The novel centrosomal regulatory protein Sec23 homolog B (SEC23B) regulates autophagy in cells, thereby providing energy and nutrients that contribute to tumor growth and distant metastasis. However, whether this role is involved in the mechanism of infiltrative metastasis in breast cancer is unclear. The aim of this study was to investigate the molecular mechanism by which SEC23B promotes breast cancer infiltration and metastasis. Methods: The association between SEC23B expression and breast cancer prognosis and metastasis was analyzed using Kaplan-Meier Plotter database and HCMDB database. MCF-7 cells were divided into vector group (control) and SEC23B overexpression plasmid group (SEC23B), and MDA231-LM2 cells were divided into SEC23B knockdown group (sh-SEC23B) and control group (sh-NC). Western blot was used to detect the expressions of SEC23B, autophagy-associated proteins [dead bone fragment 1 (SQSTM1, p62), microtubule-associated-protein light-chain-3 (LC3)] and extracellular-regulated protein kinases (ERK)/mammalian target of rapamycin (mTOR) pathway proteins in breast cancer cells. Cell migration was assessed by transwell assay and wound healing assay, and autophagic granules in cells were detected by immunofluorescence staining. In addition, an in vivo intraperitoneal tumor model was constructed to study the effect of SEC23B on breast cancer cell metastasis in vivo. Results: The overall survival of breast cancer patients with high SEC23B expression was significantly shorter than that of patients with low SEC23B expression. The expression of SEC23B in metastatic breast cancer was significantly higher than that in breast cancer without metastasis. SEC23B protein levels were lower in primary breast cancer cells (MCF-7, BT-549, MDA-MB-468 and MDA-MB-453) than in metastatic breast cancer cells (MDA231- LM2 and ZR-75-30). Compared with the control group, the SEC23B group significantly accelerated cell migration (P<0.001). Compared with the sh-NC group, the sh-SEC23B group significantly reduced cell migration (P<0.001). Compared with the control group, the expression level of LC3A/B and the formation of autophagy particles in the SEC23B group were significantly increased, while the expression of p62 protein and the phosphorylation levels of mTOR and ERK were decreased. Compared with the sh-NC group, the LC3A/B expression level and the formation of autophagy particles were significantly decreased in the sh-SEC23B group, and the phosphorylation levels of mTOR and ERK were increased, especially under starvation conditions. In in vivo experiments, tumor weight was significantly lower in the sh-SEC23B group compared with the sh-NC group (P<0.01), and there was an increase in necrotic tissue and a decrease in tumor metastasis in lung tissue in mice. sh-SEC23B group mice had a significantly lower number of lung metastatic tumors and LC3 immunohistochemical staining than the sh-NC group (P<0.01). Conclusions: SEC23B induces breast cancer autophagy and promotes cancer cell metastasis by inhibiting ERK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Objective: To study the differential expression of CELF6 in breast cancer and normal tissues and its prognostic significance in breast cancer. Methods: The expression of CELF6 in breast cancer tissues and normal breast tissues was analyzed by GEPIA. The clinical samples of breast cancer were used to study the expression level of CELF6 protein in breast cancer tissues compared with nomal tissues. KM-plotter was used to study the relationship between the expression of CELF6 and the prognosis survival of breast cancer patients. The effect of different CELF6 expression levels on the growth and proliferation of breast cancer cells was analyzed by CCK8 cell counting assay. Results: GEPIA online software analysis showed that CELF6 expression was significantly lower in breast cancer than in normal tissues (P<0.001). The results of immunohistochemistry showed that the positive expression of CELF6 in breast cancer tissues was significantly lower than that in normal tissues adjacent to cancer. The survival curve of KM-plotter online analysis showed that the survival prognosis of patients with high expression of CELF6 was significantly better than those with low expression (P<0.001). The CCK8 assay showed that the expression of CELF6 in the breast cancer cell line MDA-MB-231 was knocked down, the cell proliferation rate was significantly faster, and the proliferation rate of MDA-MB-231 cells overexpressing CELF6 was slowed down.Conclusions: CELF6 may be a potential tumor suppressor gene, which is lowly expressed in breast cancer tissues and is associated with poor prognosis in breast cancer patients. [ABSTRACT FROM AUTHOR]