本研究旨在探讨hsa-miR-497-3p对三阴性乳腺癌（TNBC）细胞行为的影响及机制。我们利用定量荧光聚合酶链反应（PCR）方法评估了从TNBC或卵泡乳腺癌（BrCa）患者获得的组织样本中Hsa-miR-497-3p的表达情况。我们将hsa-miR-497-3p模拟物和NC转染到MDA-MB-231细胞中，而将hsa-miR-497-3p抑制物和NC转染到TNBC细胞中。为了评估hsa-miR-497-3p表达水平对TNBC细胞增殖、侵袭和迁移的影响，我们采用了MTT、克隆形成、Transwell和伤口愈合实验。我们利用q-PCR和western blot来验证hsa-miR-497-3p在TNBC细胞上皮间质转化（EMT）中的作用。为了确认hsa-miR-497-3p和ZEB1之间的靶向关系，我们进行了荧光素酶测定、q-PCR和western blot分析。我们发现，与卵泡BrCa组织和细胞系相比，hsa-miR-497-3p表达在TNBC组织和细胞系中均下调。此外，hsa-miR-497-3p过表达抑制了MDA-MB-231 TNBC细胞的功能，并降低了vimentin和N-钙粘附蛋白的mRNA和蛋白表达，同时上调了E-钙粘蛋白表达。我们的结果表明，hsa-miR-497-3p通过靶向ZEB1调控TNBC细胞中的EMT，通过抑制ZEB1来调节vimentin、N-钙粘蛋白和E-钙粘蛋白的表达。总体而言，我们的研究表明，hsa-miR-497-3p通过调节EMT通过ZEB1靶向来抑制TNBC细胞的增殖和侵袭。

This study aimed to examine the hsa-miR-497-3p effect and mechanism on the behavior of triple-negative breast cancer (TNBC) cells. We evaluated the expression of Hsa-miR-497-3p in tissue samples obtained from patients diagnosed with TNBC or luminal breast cancer (BrCa), utilizing the quantitative fluorescence polymerase chain reaction (PCR) method. We transfected hsa-miR-497-3p mimics and NC into MDA-MB-231 cells, whilehsa-miR-497-3p inhibitor and NC into TNBC cells, respectively. To examine the impact of hsa-miR-497-3p expression level on TNBC cell proliferation, invasion, and migration, we employed MTT, clone formation, Transwell, and wound healing assays. We utilized both q-PCR and western blot to validate the role of hsa-miR-497-3p in the epithelial-mesenchymal transition (EMT) of TNBC cells. To confirm the targeting relationship between hsa-miR-497-3p and ZEB1, we performed luciferase assays, q-PCR, and western blot analysis. We found that the hsa-miR-497-3p expression was down-regulated in both TNBC tissues and cell lines in comparison to luminal BrCa tissues and cell lines. Furthermore, hsa-miR-497-3p overexpression hindered the cell function of TNBC cells MDA-MB-231, while downregulating the mRNA and protein expression of vimentin and N-cadherin, while simultaneously upregulating E-cadherin expression. Our results demonstrate that hsa-miR-497-3p regulates EMT in TNBC cells through ZEB1 targeting, as evidenced by the modulation of the expression of vimentin, N-cadherin, and E-cadherin via ZEB1 inhibition. Overall, our study suggests that hsa-miR-497-3p inhibits the proliferation and invasion of TNBC cells through the modulation of EMT via ZEB1 targeting.