Downregulation of UPK1A suppresses proliferation and enhances apoptosis of bladder transitional cell carcinoma cells

被引:0
作者
Haiyan Zhu
Yuxin Tang
Xiangyang Zhang
Xianzhen Jiang
Yong Wang
Yu Gan
Jianfu Yang
机构
[1] Central South University,Department of Anesthesiology, The Third Xiangya Hospital
[2] Central South University,Department of Urology, The Third Xiangya Hospital
[3] Central South University,Department of Urology, Xiangya Hospital
[4] University of Illinois at Chicago,Andrology Laboratory, Department of Urology
来源
Medical Oncology | 2015年 / 32卷
关键词
Antisense nucleotides; UPK1A; Proliferation; Apoptosis; Transitional cell carcinoma;
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摘要
Uroplakin 1A (UPK1A) is a specific marker of mammalian urothelium and one of major proteins contained in urothelial plaques. Many recent studies reported that UPK1A could be useful marker for diagnosis, detection and prognostic prediction of transitional cell carcinoma. However, relatively little is known about its exact roles in bladder transitional cell carcinoma (BTCC). We tried to explore the roles UPK1A plays in BTCC via the transfection of its antisense nucleotides (AS) into T24 cells to observe their changes of proliferation and apoptosis. After AS was successfully transfected into T24 cells, the percentages of proliferating T24 cells at 24 and 48 h after the treatment were 57.2 ± 6.8 and 44.7 ± 5.2 %, significantly lower than that of control group, as shown by MTT (p < 0.05 and 0.01). At 24 h after transfection of AS, the percentage of apoptotic T24 cells was 26.87 % measured by flow cytometry, significantly higher than that of control group (p < 0.01). Similarly, Hoechst 33258 staining showed that the percentage of apoptotic nuclei of T24 cells after 24 h treated by AS was 28.9 %, significantly higher than that of control (p < 0.05). The most common and typical morphological changes of apoptosis, including shrink, pyknosis and karyorrhexis of T24 cells nuclei and DNA fragmentation were seen from Hoechst 33258 staining and DNA agarose gel electrophoresis. Taken together, inhibition of UPK1A can suppress proliferation and enhance apoptosis of BTCC T24 cells, suggesting it a potential target to treat this disease.
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