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LASS2在裸鼠模型中调节膀胱癌细胞致瘤性的作用。

The role of LASS2 in regulating bladder cancer cell tumorigenicity in a nude mouse model.

作者信息

Chen Yujin, Wang Haifeng, Xiong Tao, Zou Renchao, Tang Zhaoran, Wang Jiansong

机构信息

Department of Urology, The Second Affiliated Hospital of Kunming Medical University, Yunnan Institute of Urology, Kunming, Yunnan 650101, P.R. China.

Department of Nephrology, Chuxiong People's Hospital, Chuxiong, Yunnan 675000, P.R. China.

出版信息

Oncol Lett. 2017 Nov;14(5):5149-5156. doi: 10.3892/ol.2017.6880. Epub 2017 Sep 4.

Abstract

Previous studies have demonstrated that LAG1 longevity assurance homolog 2 (LASS2) is a novel tumor suppressor gene that is significantly associated with the proliferation and invasion ability of tumor cells. However, the role LASS2 serves in regulating bladder cancer cell tumorigenicity and tumor growth has not yet been elucidated in animal or clinical studies. In the present study, LASS2 knockdown in human bladder cancer EJ-M3 cells significantly promoted the growth of xenografts in nude mice compared with the control group, while overexpression of LASS2 suppressed tumor growth; however, this was not statistically significant. Furthermore, LASS2 knockdown resulted in more apparent heteromorphism and a higher activity of matrix metalloproteinase (MMP)-2 and MMP-9 in xenograft tumors. The data from the present study demonstrated that LASS2 knockdown significantly promoted the tumorigenicity and growth of EJ-M3 xenograft tumors in nude mice, and that LASS2 overexpression has a tendency to inhibit the growth of xenografts, suggesting that it may be a potential therapeutic target for bladder cancer.

摘要

先前的研究表明,LAG1寿命保证同源物2(LASS2)是一种新型肿瘤抑制基因,与肿瘤细胞的增殖和侵袭能力显著相关。然而,LASS2在调节膀胱癌细胞致瘤性和肿瘤生长中所起的作用在动物或临床研究中尚未阐明。在本研究中,与对照组相比,人膀胱癌EJ-M3细胞中LASS2基因敲低显著促进了裸鼠体内异种移植瘤的生长,而LASS2过表达则抑制了肿瘤生长;然而,这一结果无统计学意义。此外,LASS2基因敲低导致异种移植瘤中更明显的异型性以及基质金属蛋白酶(MMP)-2和MMP-9的活性更高。本研究数据表明,LASS2基因敲低显著促进了裸鼠体内EJ-M3异种移植瘤的致瘤性和生长,而LASS2过表达有抑制异种移植瘤生长的趋势,提示其可能是膀胱癌的一个潜在治疗靶点。

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