Department of General Surgery, Shanghai Seventh People's Hospital, Shanghai, P.R. China.
Central Laboratory, Shanghai Seventh People's Hospital, Shanghai, P.R. China.
J Recept Signal Transduct Res. 2022 Feb;42(1):1-8. doi: 10.1080/10799893.2020.1837871. Epub 2020 Oct 26.
This study mainly aimed to explore the influences of Calcium Voltage-Gated Channel Subunit Alpha1 B (CACNA1B) on the development of breast cancer and the related mechanism.
The information of patients with breast cancer from TCGA database was used for analyses of CACNA1B expression and its prognostic value. Loss- and gain- of functions of CACNA1B were conducted in MCF7 and Bcap-37 cells, respectively. CCK-8, colony formation and transwell assays were applied for evaluating the cell viability and motility. Western blot was used for protein expression detection.
We revealed that highly expressed CACNA1B in breast cancer tissues was related to poor prognosis according to the data gained from TCGA database. The outcomes of functional assays showed that depletion of CACNA1B restrained MCF7 cell growth, invasion and migration and high-expression of CACNA1B fortified the growth, invasion and migration in Bcap-37 cells. Finally, we manifested that silencing CACNA1B obviously raised the protein expression level of E-cadherin and reduced the protein levels of Cyclin D1, N-cadherin and Snail in MCF7 cells, whilst, over-expression of CACNA1B reduced the level of E-cadherin and increased the expression of Cyclin D1, N-cadherin and Snail in Bcap-37 cells.
These results identified CACNA1B as a forwarder of the growth, invasion and migration in breast cancer cells.
本研究主要旨在探讨钙电压门控通道亚基 α1 B（CACNA1B）对乳腺癌发展的影响及其相关机制。
利用 TCGA 数据库中乳腺癌患者的信息，分析 CACNA1B 的表达及其预后价值。分别在 MCF7 和 Bcap-37 细胞中进行 CACNA1B 的缺失和功能获得实验。应用 CCK-8、集落形成和 Transwell 实验评估细胞活力和迁移能力。采用 Western blot 检测蛋白表达。
根据 TCGA 数据库获得的数据，我们发现乳腺癌组织中高表达的 CACNA1B 与预后不良有关。功能实验的结果表明，CACNA1B 的缺失抑制了 MCF7 细胞的生长、侵袭和迁移，而 CACNA1B 的高表达增强了 Bcap-37 细胞的生长、侵袭和迁移。最后，我们发现沉默 CACNA1B 明显提高了 MCF7 细胞中 E-钙黏蛋白的蛋白表达水平，降低了 Cyclin D1、N-钙黏蛋白和 Snail 的蛋白水平，而 CACNA1B 的过表达则降低了 E-钙黏蛋白的水平，并增加了 Bcap-37 细胞中 Cyclin D1、N-钙黏蛋白和 Snail 的表达。
这些结果表明 CACNA1B 是乳腺癌细胞生长、侵袭和迁移的促进因子。
