CAJ | 학술논문

目的：：明确S100 A16在前列腺癌中的表达水平，并探讨它在前列腺癌细胞侵袭中的作用及分子机制。方法：利用Western blot和免疫组化的方法检测S100 A16在人类前列腺癌组织中的表达；构建S100 A16过表达及干扰细胞模型，利用侵袭实验，研究S100 A16对前列腺癌细胞侵袭潜能的影响；通过检测p53下游基因p21和p27信号通路，初步探讨S100 A16在前列腺癌细胞侵袭过程中的分子机制。结果：S100 A16在前列腺癌组织中高表达，免疫组化结果提示S100 A16的表达水平与前列腺癌的Gleason评分相关，并且主要位于细胞核内。 S100 A16能够促进前列腺癌细胞侵袭。过表达S100 A16使细胞周期依赖性激酶抑制因子p21/p27的表达下降，而下调S100 A16的表达则增加p21/p27的表达。结论：S100 A16在前列腺癌组织中高表达，并与前列腺癌的临床分期正相关；S100 A16促进前列腺癌细胞侵袭；S100 A16可能通过抑制p21的表达促进前列腺癌细胞的侵袭。
목적：：명학S100 A16재전렬선암중적표체수평，병탐토타재전렬선암세포침습중적작용급분자궤제。방법：이용Western blot화면역조화적방법검측S100 A16재인류전렬선암조직중적표체；구건S100 A16과표체급간우세포모형，이용침습실험，연구S100 A16대전렬선암세포침습잠능적영향；통과검측p53하유기인p21화p27신호통로，초보탐토S100 A16재전렬선암세포침습과정중적분자궤제。결과：S100 A16재전렬선암조직중고표체，면역조화결과제시S100 A16적표체수평여전렬선암적Gleason평분상관，병차주요위우세포핵내。 S100 A16능구촉진전렬선암세포침습。과표체S100 A16사세포주기의뢰성격매억제인자p21/p27적표체하강，이하조S100 A16적표체칙증가p21/p27적표체。결론：S100 A16재전렬선암조직중고표체，병여전렬선암적림상분기정상관；S100 A16촉진전렬선암세포침습；S100 A16가능통과억제p21적표체촉진전렬선암세포적침습。
Objective:To examine the expression of S100A16 in prostate cancer(PC) specimens, and investigated the effects and mechanisms of S100A16 on PC cell proliferation and invasion. Methods: We examined the expression of S100A16 in PC specimens and prostate cancer cell lines by Western blot and immunohistochemistry. In vitro, we constructed cells forcing S100A16 expression as well as depletion of S100A16 to investigate the role of S100A16 on cell invasion assay. p21/p27, the downstream of p53 were tested to elucidate the mechanism of S100A16 on PC progression. Results: The expression of S100A16 was higher in PC and PC cell lines than in normal prostate tissues and prostate epithelial cell respectively. Immunohistochemical staining showed that S100A16 expression level was significantly correlated with Gleason scores. Simultaneously, S100A16 was mainly localized in the nucleus. Depletion of S100A16 using shRNA significantly reduced the cell growth, migration, invasion capability. Forcing S100A16 expression may decrease the expression of the cyclin-dependent kinase inhibitors (p21, p27), while suppression of the S100A16 gene increased p21/p27 expression. Conclusion: S100A16 was overexpressed in human prostate cancer and PC cell lines, and the level of S100A16 was positively correlated with the cell malignant degree. Upregulation of S100A16 promoted the cell invasion capability. S100A16 may control invasive potential of human PC cells by mediating the expression of p21/p27 signaling pathways.