Metastasis is the major cause of mortality in patients with breast cancer. Understanding the metastatic mechanism to guide clinical diagnoses and the treatment of breast cancer remains a challenge. We found that the expression of Mex-3 RNA binding family member A (MEX3A) was upregulated significantly and related to tumor grade in breast cancer. The results of in vitro and in vivo studies showed that knockdown of MEX3A inhibited the metastasis and impaired the stemness of breast cancer cells. Furthermore, activation of the β-catenin signaling pathway was discovered as a molecular intermediate of MEX3A-mediated regulation. We also found that ectopic expression of β-catenin restored the migration ability, invasion ability, and CD44⁺/CD24^- percentage of MDA-MB-231 and BT549 cells when MEX3A was depleted. In addition, we revealed that MEX3A positively regulated the expression of β-catenin by downregulating Dickkopf WNT signaling pathway inhibitor 1 (DKK1) expression. Therefore, a previously undiscovered role of MEX3A comprising a critical contribution to promoting metastasis and maintaining the stemness of breast cancer via the Wnt/β-catenin pathway was demonstrated in the present study.

转移是乳腺癌患者死亡的主要原因。了解转移机制以指导临床诊断和乳腺癌的治疗仍然是一个挑战。我们发现Mex-3 RNA结合家族成员A（MEX3A）的表达显着上调并与乳腺癌的肿瘤分级有关。结果在体外和体内研究表明MEX3A的敲低抑制转移和受损乳腺癌细胞的干性。此外，β-连环蛋白信号通路的激活被发现是 MEX3A 介导的调节的分子中间体。我们还发现 β-catenin 的异位表达恢复了迁移能力、侵袭能力和 CD44 ⁺ /CD24 ^-当 MEX3A 耗尽时 MDA-MB-231 和 BT549 细胞的百分比。此外，我们发现 MEX3A 通过下调 Dickkopf WNT 信号通路抑制剂 1（DKK1）的表达来正调节 β-catenin 的表达。因此，本研究证明了 MEX3A 以前未被发现的作用，包括通过 Wnt/β-catenin 途径促进转移和维持乳腺癌干性的关键贡献。