HSDL2 Promotes Bladder Cancer Growth In Vitro and In Vivo
HSDL2 Promotes Bladder Cancer Growth In Vitro and In Vivo
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DOI：
10.7150/ijms.31288
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发表时间：
2019-01-01
影响因子：
3.6
通讯作者：
Li, Qiu-Gen
中科院分区：
文献类型：
--
作者：
Jia, Ling-Hua;Hu, Mei-Di;Li, Qiu-Gen
膀胱癌是泌尿系常见的恶性肿瘤，膀胱癌患者预后差。过氧化物酶体中的脂质代谢异常参与肿瘤进展。位于过氧化物酶体中的羟基类固醇脱氢酶样2（HSDL2）调节脂肪酸合成。在本研究中，我们报道了与正常人尿路上皮细胞相比，两种人膀胱癌细胞系5637和T24中的HSDL2上调。慢病毒介导的HSDL2基因敲减可抑制人膀胱癌T24细胞的增殖和集落形成，促进细胞凋亡。在裸鼠中，HSDL2敲低抑制体内T24衍生的异种移植物的生长。总之，我们的研究结果表明，HSDL2在膀胱癌中发挥致癌作用，并可能作为膀胱癌治疗的潜在靶点。
Bladder cancer is a common malignant urinary tumor, and patients with bladder cancer have poor prognosis. Abnormal lipid metabolism in peroxisomes is involved in tumor progression. Hydroxysteroid dehydrogenase-like 2 (HSDL2) localized in peroxisomes regulates fatty acid synthesis. In the present study, we reported that HSDL2 was upregulated in two human bladder cancer cell lines 5637 and T24 compared to normal human urothelial cells. Furthermore, lentiviral-mediated HSDL2 knockdown inhibited the proliferation and colony formation while promoted the apoptosis of human bladder cancer T24 cells in vitro. In nude mice HSDL2 knockdown inhibited the growth of T24 derived xenografts in vivo. In conclusion, our results suggest that HSDL2 plays an oncogenic role in bladder cancer and might serve as a potential target for bladder cancer therapy.