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Osteopontin accelerates the development and metastasis of bladder cancer via activating JAK1/STAT1 pathway.
Genes & Genomics ( IF 2.1 ) Pub Date : 2020-02-22 , DOI: 10.1007/s13258-019-00907-6
Na Zhang 1 , Fei Li 1 , Juanyu Gao 2 , Shibao Zhang 1 , Qihong Wang 1
Affiliation  

BACKGROUND Bladder cancer is the 10th common cancer worldwide. Osteopontin has been found to enhance cell proliferation, metastasis and invasion in various human tumors. OBJECTIVE To investigate the roles of osteopontin in bladder cancer. 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. 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. 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.

中文翻译:

骨桥蛋白通过激活JAK1 / STAT1途径加速膀胱癌的发展和转移。

背景技术膀胱癌是全球第十大常见癌症。已经发现骨桥蛋白增强了各种人类肿瘤中的细胞增殖,转移和侵袭。目的探讨骨桥蛋白在膀胱癌中的作用。方法在膀胱癌细胞系(T24和SCaBER)中进行RNA干扰和骨桥蛋白的过表达。使用CCK-8测定法和流式细胞仪分别测量细胞增殖和凋亡。使用transwell测定法确定细胞侵袭。结果与邻近的正常组织相比,骨桥蛋白在膀胱癌组织中高表达。其高表达与高组织学分级,高TNM分期(III和IV)和不良预后密切相关。对于具有骨桥蛋白干扰的T24细胞和具有骨桥蛋白过度表达的SCaBER细胞,细胞增殖分别被显着抑制(3.58倍对5.62倍)和增强(7.81倍对5.29倍)。T24细胞的凋亡部分从4.48%显着增加到10.75%,而SCaBER细胞的凋亡部分从7.33%显着下降到4.01%。侵袭的T24和SCaBER细胞分别显着减少至52.0%和增加至2.0倍。骨桥蛋白的过表达增强了两个细胞系中JAK1和STAT1的表达(1.54倍和2.39倍; 2.33倍和2.05倍)和激活(1.80倍和1.96倍; 2.00倍和2.59倍)。膀胱癌。结论骨桥蛋白可能促进膀胱癌和骨桥蛋白的增殖,抑制细胞凋亡并加速侵袭,从而促进膀胱癌的发展和转移。
更新日期:2020-02-22
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