Osteopontin accelerates the development and metastasis of bladder cancer via activating JAK1/STAT1 pathway

骨桥蛋白通过激活JAK1/STAT1通路加速膀胱癌的发展和转移

阅读:7
作者:Na Zhang, Fei Li, Juanyu Gao, Shibao Zhang, Qihong Wang

Background

Bladder cancer is the 10th common cancer worldwide. Osteopontin has been found to enhance cell proliferation, metastasis and invasion in various human tumors.

Conclusion

Osteopontin might enhance proliferation, inhibit apoptosis and accelerate invasion and thus promote the development and metastasis of bladder cancer, and osteopontin's functions might be mediated by activating JAK1/STAT1 signaling pathway.

Methods

The RNA interference and overexpression of osteopontin were performed in bladder cancer cell lines (T24 and SCaBER). Cell proliferation and apoptosis were measured using CCK-8 assay and flow cytometry, respectively. Cell invasion was determined using transwell assay.

Objective

To investigate the roles of osteopontin in bladder cancer.

Results

Osteopontin was highly expressed in bladder cancer tissues in comparison with the adjacent normal tissues. Its high expression significantly correlated with high histologic grade, high TNM stage (III and IV) and poor prognosis. For T24 cells with osteopontin interference and SCaBER cells with osteopontin overexpression, cell proliferation was significantly inhibited (3.58-fold vs. 5.62-fold) and enhanced (7.81-fold vs. 5.29-fold), respectively. The apoptosis portion of T24 cells significantly increased from 4.48 to 10.75%, and that of SCaBER cells significantly declined from 7.33 to 4.01%. The invaded T24 and SCaBER cells significantly decreased to 52.0% and increased to 2.0-fold, respectively. Osteopontin overexpression enhanced the expression (1.54-fold and 2.39-fold; 2.33-fold and 2.05-fold) and activation (1.80-fold and 1.96-fold; 2.00-fold and 2.59-fold) of JAK1 and STAT1 in two cell lines of bladder cancer.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。