C6orf106 enhances NSCLC cell invasion by upregulating vimentin, and downregulating E-cadherin and P120ctn
C6orf106 enhances NSCLC cell invasion by upregulating vimentin, and downregulating E-cadherin and P120ctn
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C6orf106 通过上调波形蛋白并下调 E-钙粘蛋白和 P120ctn 增强 NSCLC 细胞侵袭
DOI：
10.1007/s13277-015-3274-9
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Wang Enhua
中科院分区：
文献类型：
--
作者：
Zhang Xiupeng;Miao Yuan;Yu Xinmiao;Zhang Yong;Jiang Guiyang;Liu Yang;Yu Juanhan;Han Qiang;Zhao Huanyu;Wang Enhua
6号染色体开放阅读框106（C6orf106）是一种新发现的蛋白质；其在人类肿瘤中的表达和临床病理意义仍不清楚。采用免疫组织化学、蛋白质印迹和免疫荧光来评估非小细胞肺癌 (NSCLC) 中 C6orf106 的表达。此外，还分析了亚细胞定位与临床病理因素之间的关系。通过C6orf106在肺癌细胞系中的过表达和抑制，我们探讨了该分子对NSCLC侵袭能力的影响。与癌旁正常肺组织相比，C6orf106 在肺癌组织细胞的细胞质中高表达 (60.4%, 75/124) (15.2%, 7/46,p<0.001)。此外，其表达与分化程度（p= 0.001）、TNM分期（p= 0.011）、淋巴结转移（p= 0.018）和不良预后（p= 0.006）呈正相关。此外，C6orf106 过表达增强了 NSCLC 细胞的侵袭。此外，C6orf106 被证明可以增加波形蛋白的表达，同时减少 E-钙粘蛋白和 P120ctn 的表达。 C6orf106在NSCLC中高表达，与临床病理因素以及不良预后相关。 C6orf106 促进 NSCLC 细胞的侵袭。最后，C6orf106 上调波形蛋白，下调 E-钙粘蛋白和 P120ctn。
Chromosome 6 open reading frame 106 (C6orf106) is a newly discovered protein; its expression and clinical pathological significance in human tumors remains unclear. Immunohistochemistry, Western blot, and immunofluorescence were performed to assess C6orf106 expression in non-small cell lung cancer (NSCLC). In addition, the relationships between subcellular localization and clinical pathological factors were analyzed. Through C6orf106 overexpression and repression, respectively, in lung cancer cell lines, we explored the effect of this molecule on NSCLC invasion abilities. C6orf106 was highly expressed in the cytoplasm of lung cancer tissue cells (60.4 %, 75/124), compared with adjacent normal lung tissues (15.2 %, 7/46,p< 0.001). In addition, its expression was positively correlated with differentiation (p= 0.001), TNM stage (p= 0.011), lymph node metastasis (p= 0.018), and poor prognosis (p= 0.006). Furthermore, C6orf106 overexpression enhanced NSCLC cell invasion. Moreover, C6orf106 was shown to increase vimentin expression, while decreasing E-cadherin and P120ctn. C6orf106 is highly expressed in NSCLC and correlates with clinical and pathological factors, as well as poor prognosis. C6orf106 promotes invasion in NSCLC cells. Finally, C6orf106 upregulates vimentin, and downregulates E-cadherin and P120ctn.