Zhang Jun, He Jiejie, Qiang Ziyang, Zhang Junli, Hao Fengchen, Song Shiqi, Chen Xiuying, Ma Wei, Li Yan
Department of Urology Surgery, Affiliated Hospital of Qinghai University, No. 29, Tongren Road, West of the City, Xining, 810000, Qinghai, China.
Department of Gynecologic Surgery, Affiliated Hospital of Qinghai University & Affiliated Cancer Hospital of Qinghai University, No. 29, Tongren Road, West of the City, Xining, 810000, Qinghai, China.
Open Life Sci. 2024 Dec 18;19(1):20220981. doi: 10.1515/biol-2022-0981. eCollection 2024.
Bladder cancer (BC) is the tenth most common tumor worldwide, characterized by high incidence rates and mortality. This study aimed to explore the role of Methyltransferase like 13 (METTL13) in BC cells. J82 and T24 cells were cultured for experiments. Cell viability, migration, and invasion were assessed using CCK-8 and transwell assays. Senescence-associated beta-galactosidase (SA-β-gal) levels were detected using a β-galactosidase staining kit. METTL13 and cell cycle-related protein levels were quantified using RT-qPCR and Western blotting. The results showed that METTL13 was upregulated in BC cells. Silencing METTL13 decreased cell viability, migration, and invasion in BC cells, whereas METTL13 overexpression increased these parameters. Additionally, METTL13 knockdown inhibited the phosphorylation levels of PI3K, AKT, and mTOR. Inhibition of the PI3K/AKT pathway reversed the effects of METTL13 on cell viability, migration, invasion, and cell cycle-related proteins in BC cells. experiments showed that METTL13 knockdown inhibited tumor growth and development. In conclusion, this study demonstrated that METTL13 promoted the malignant behaviors of BC cells through activation of the PI3K/AKT signaling pathway. METTL13 may be a promising therapeutic target for BC in the future.
膀胱癌（BC）是全球第十大常见肿瘤，具有高发病率和死亡率的特点。本研究旨在探讨甲基转移酶样13（METTL13）在膀胱癌细胞中的作用。培养J82和T24细胞用于实验。使用CCK - 8和Transwell实验评估细胞活力、迁移和侵袭能力。使用β - 半乳糖苷酶染色试剂盒检测衰老相关β - 半乳糖苷酶（SA - β - gal）水平。使用RT - qPCR和蛋白质免疫印迹法对METTL13和细胞周期相关蛋白水平进行定量分析。结果显示，METTL13在膀胱癌细胞中表达上调。沉默METTL13可降低膀胱癌细胞的活力、迁移和侵袭能力，而METTL13过表达则增加这些参数。此外，敲低METTL13可抑制PI3K、AKT和mTOR的磷酸化水平。抑制PI3K/AKT信号通路可逆转METTL13对膀胱癌细胞活力、迁移、侵袭及细胞周期相关蛋白的影响。实验表明，敲低METTL13可抑制肿瘤生长和发展。总之，本研究表明METTL13通过激活PI3K/AKT信号通路促进膀胱癌细胞的恶性行为。METTL13未来可能成为膀胱癌有前景的治疗靶点。
