膀胱癌（BC）细胞表现出高水平的自噬活性，有助于形成细胞的保护机制，以抵御目前的治疗方法。Hsa-microRNA-34a（miR-34a）在多种癌症中具有抗肿瘤功能。然而，miR-34a在调节BC的肿瘤侵袭性和保护性自噬的功能机制仍然大部分未知。首先，将miR-34a mimic转染到BC细胞中，通过免疫荧光染色显示LC3-II和p62的积累。结果表明，需要用于自噬体-溶酶体融合的语法素17（STX17）在miR-34a mimic处理后下调。在机制上，miR-34a减少STX17蛋白的表达，该蛋白直接结合于STX17 3'‑非翻译区域，从而抑制STX17 mRNA的翻译，最终抑制BC中的保护性自噬。细胞活力和克隆形成实验显示，在BC细胞中过表达miR-34a可增强顺铂、阿霉素、艾匹霉素和丝裂霉素C的化疗敏感性。此外，miR-34a通过抑制cyclin D1和cyclin E2蛋白的表达，抑制细胞增殖并引发G0/G1细胞周期阻滞。此外，miR-34a通过下调上皮-间充质转化来抑制细胞运动性。综上所述，miR-34a抑制BC中的细胞增殖、运动性和自噬活性，有益于BC的治疗。

Bladder cancer (BC) cells exhibit a high basal level of autophagy activity, which contributes to the development of a protective mechanism for cellular survival against current treatments. Hsa‑microRNA‑34a (miR‑34a) presents anti‑tumor function in several types of cancer. However, the functional mechanism of miR‑34a in regulating tumor aggressiveness and protective autophagy of BC remains largely unknown. First, transfected BC cells with miR‑34a mimic exhibited LC3‑II and p62 accumulation through immunofluorescence staining. It was demonstrated that syntaxin 17 (STX17), which is required for autophagosome‑lysosome fusion, was downregulated upon miR‑34a mimic treatment. Mechanistically, miR‑34a reduced the expression of STX17 proteins that directly bind on STX17 3'‑untranslated regions and thus suppressed STX17 mRNA translation to eventually inhibit protective autophagy in BC. Cell viability and colony formation assays revealed that overexpression of miR‑34a in BC cells enhances the chemosensitivity of cisplatin, doxorubicin, epirubicin and mitomycin C. Furthermore, miR‑34a inhibited cell proliferation and triggered G0/G1 cell cycle arrest by inhibiting cyclin D1 and cyclin E2 protein expression. Moreover, miR‑34a suppressed cell motility through the downregulation of epithelial‑mesenchymal transition. In summary, miR‑34a inhibits cell proliferation, motility and autophagy activity in BC, which can benefit BC treatment.