Overexpression of miR-340 inhibits cell proliferation and induces apoptosis of human bladder cancer via targeting Glut-1

• Published in: BMC urology 2021-12, Vol.21 (1), p.168-168, Article 168
• Main Authors: Xu, Gang, Pan, Shouhua, Zhu, Zhirong, Li, Junlong
• Format: Article
• Language: English
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Antibodies; Apoptosis; Apoptosis - genetics; Binding sites; Bioinformatics; Biomarkers; Bladder cancer; Bone cancer; Cell growth; Cell proliferation; Cell Proliferation - genetics; Cholecystokinin; Development and progression; Disease; Flow cytometry; Gene expression; Gene Expression Regulation, Neoplastic; Glucose Transporter Type 1 - physiology; Glut-1; Health aspects; Humans; Metastases; Metastasis; MicroRNA; MicroRNAs; MicroRNAs - genetics; miR-340; miRNA; Mortality; Proliferating cell nuclear antigen; Proliferation; Proteins; Tumor Cells, Cultured; Tumor suppressor genes; Tumors; Urinary Bladder Neoplasms - genetics; Urinary Bladder Neoplasms - pathology; Urology; Western blotting
• ISSN: 1471-2490; 1471-2490
• DOI: 10.1186/s12894-021-00935-z

Bladder cancer (BC) has high mortality due to distant metastasis. Previous works suggested that microRNA (miRNA)-340 is a critical regulator for the development and progression of various cancers. The specific biological function of miR-340 in BC is little known. In the present study, RT-qPCR was performed to measure the expression of miR-340 in paired BC tissues and adjacent non-tumor tissues. Next, the target gene of miR-340 was identified using dual-luciferase reporter assay and its level was also tested in tissues. Moreover, cell proliferation and apoptosis were analyzed by CCK-8 and flow cytometry. Finally, the expression of PCNA, Bax was detected by RT-qPCR and western blotting, as well as PI3K/AKT signaling measured by western blotting. The results demonstrated that miR-340 expression was downregulated and its target Glut-1 level was upregulated in BC tissues. Functionally, overexpression of miR-340 suppressed the proliferation and induced apoptosis in BC cells, while Glut-1 reversed the suppression of proliferation or induction of apoptosis induced by miR-340. Additionally, miR-340 repressed PCNA, p-PI3K and p-AKT levels but enhanced Bax level, while Glut-1 rescued the effects. In conclusion, miR-340 functions as a tumor suppressor of BC, which inhibited proliferation and induced apoptosis by targeting Glut-1 partly through regulating PCNA, Bax expression and PI3K/AKT pathway. This study suggested that miR-340 is a potential target for the treatment of BC.