Connexins (Cx), the basic subunit of gap junctions, play important roles in cell homeostasis, and their abnormal expression and function are associated with human hereditary diseases and cancers. In tumorigenesis, connexins were observed to have both anti-tumorigenic and pro-tumorigenic roles in a context- and stage-dependent manner. Initially, Cx26 and Cx43 were thought to be the only connexins involved in normal breast homeostasis and breast cancer. Later on, association of Cx32 expression with lymph node metastasis of breast cancer and subsequent demonstration of its expression in normal breast tissue suggested that Cx32 contributes to breast tissue homeostasis. Here, we aimed to determine the effects of Cx32 on normal breast cells, MCF10A, and on breast cancer cells, MDA-MB-231. Cx32 overexpression had profound effects on MCF10A cells, decreasing cell proliferation by increasing the doubling time of MCF10A. Furthermore, MCF10A cells acquired mesenchymal-like appearance upon Cx32 expression and had increased migration capacity and expression of both E-cadherin and vimentin. In contrast, Cx32 overexpression altered the EMT markers of MDA-MB-231 by increasing the expression of mesenchymal markers, such as slug and vimentin, and decreasing E-cadherin expression without affecting their proliferation and morphology. Our results indicate, for the first time in the literature, that Cx32 has tumor-promoting roles in MCF10A and MDA-MB-231 cells.

连接蛋白（Cx）是间隙连接的基本亚基，在细胞稳态中发挥着重要作用，其异常表达和功能与人类遗传性疾病和癌症有关。在肿瘤发生过程中，观察到连接蛋白以背景和阶段依赖的方式具有抗肿瘤发生和促肿瘤发生的作用。最初，Cx26 和 Cx43 被认为是参与正常乳腺稳态和乳腺癌的唯一连接蛋白。后来，Cx32 表达与乳腺癌淋巴结转移的关联以及随后在正常乳腺组织中表达的证明表明 Cx32 有助于乳腺组织稳态。在这里，我们的目的是确定 Cx32 对正常乳腺细胞 MCF10A 和乳腺癌细胞 MDA-MB-231 的影响。 Cx32 过度表达对 MCF10A 细胞产生深远影响，通过增加 MCF10A 的倍增时间来减少细胞增殖。此外，MCF10A 细胞在 Cx32 表达后获得间充质样外观，并具有增加的迁移能力以及 E-钙粘蛋白和波形蛋白的表达。相比之下，Cx32 过表达通过增加间充质标记物（如蛞蝓和波形蛋白）的表达并减少 E-钙粘蛋白表达来改变 MDA-MB-231 的 EMT 标记物，而不影响其增殖和形态。我们的结果首次在文献中表明，Cx32 在 MCF10A 和 MDA-MB-231 细胞中具有促肿瘤作用。