Zha Zhuocen, Ge Fei, Li Na, Zhang Shijun, Wang Chenxi, Gong Fuhong, Miao Jingge, Chen Wenlin
First-Class Discipline Team of Kunming Medical University, Third Department of Breast Surgery, Peking University Cancer Hospital Yunnan, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, 650118, China.
Oncology department, Guizhou Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guiyang, Guizhou, 550000, China.
Cell Biochem Biophys. 2025 Jun;83(2):1483-1494. doi: 10.1007/s12013-024-01625-x. Epub 2024 Dec 14.
Breast cancer is a disease that seriously endangers the health of women. However, it is difficult to treat due to the emergence of metastasis and drug resistance. Exploring the metastasis mechanism of breast cancer is helpful to aim for the appropriate target. The epithelial-mesenchymal transition (EMT) is an important mechanism of breast cancer metastasis. Sodium channel 1.5(Na1.5) and the GTPase Rac1 are factors related to the degree of malignancy of breast tumors. The expression of Na1.5 and the activation of Rac1 are both involved in EMT. In addition, Na1.5 can change the plasma membrane potential (Vm) by promoting the inflow of Na to depolarize the cell membrane, induce the activation of Rac1 and produce a cascade of reactions that lead to EMT in breast cancer cells; this sequence of events further induces the movement, migration and invasion of tumor cells and affects the prognosis of breast cancer patients. In this paper, the roles of Na1.5 and Rac1 in EMT-mediated breast cancer progression were reviewed.
乳腺癌是一种严重危害女性健康的疾病。然而,由于转移和耐药性的出现,其治疗难度较大。探索乳腺癌的转移机制有助于确定合适的治疗靶点。上皮-间质转化(EMT)是乳腺癌转移的重要机制。钠通道1.5(Na1.5)和GTP酶Rac1是与乳腺肿瘤恶性程度相关的因素。Na1.5的表达和Rac1的激活均参与EMT过程。此外,Na1.5可通过促进钠离子内流改变质膜电位(Vm),使细胞膜去极化,诱导Rac1激活,并产生一系列导致乳腺癌细胞发生EMT的反应;这一系列事件进一步诱导肿瘤细胞的运动、迁移和侵袭,并影响乳腺癌患者的预后。本文综述了Na1.5和Rac1在EMT介导的乳腺癌进展中的作用。