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Y盒结合蛋白1的敲低通过逆转上皮-间质转化抑制HT-29结肠直肠腺癌细胞的恶性进展。

Knockdown of Y‑box‑binding protein‑1 inhibits the malignant progression of HT‑29 colorectal adenocarcinoma cells by reversing epithelial‑mesenchymal transition.

作者信息

Yan Xue-Bing, Zhu Qing-Chao, Chen Hong-Qi, Peng Jia-Yuan, Chao Hong-Lei, Du Hang-Xiang, Wang Zhi-Gang, Jin Zhi-Ming

机构信息

Department of Surgery, Sixth People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200233, P.R. China.

出版信息

Mol Med Rep. 2014 Nov;10(5):2720-8. doi: 10.3892/mmr.2014.2545. Epub 2014 Sep 5.

DOI:10.3892/mmr.2014.2545
PMID:25201740
Abstract

Y‑box binding protein‑1 (YB‑1) has been identified as an oncoprotein in various malignancies. The aim of this study was to investigate the biological role of YB‑1 and its association with epithelial‑to‑mesenchymal transition (EMT) in colorectal cancer (CRC). The expression of YB‑1 and three EMT‑related proteins (E‑cadherin, N‑cadherin and vimentin) was analyzed in 80 CRC and matched normal tissue samples, by immunohistochemistry. The results indicated that the expression of YB‑1 was higher in CRC tissue samples than that in matched normal controls and was significantly correlated with tumor differentiation, tumor invasion, lymph node metastasis and distant metastases. Furthermore, analysis showed that YB‑1 expression was negatively correlated with E‑cadherin and positively correlated with N‑cadherin and vimentin expression. In vitro assays showed that knockdown of YB‑1 inhibited the proliferation, apoptosis resistance, invasion and migration of the HT‑29 CRC cell line. Of note, following knockdown of YB‑1, E‑cadherin expression was elevated whereas N‑cadherin and vimentin expression was reduced. Taken together, these results suggest that YB‑1 promotes the malignant progression of CRC in part through the induction of EMT, and YB‑1 may therefore be a potential novel target for CRC treatment.

摘要

Y盒结合蛋白1(YB-1)已被确定为多种恶性肿瘤中的一种癌蛋白。本研究的目的是探讨YB-1在结直肠癌(CRC)中的生物学作用及其与上皮-间质转化(EMT)的关系。采用免疫组织化学方法分析了80例CRC组织及其配对正常组织样本中YB-1和三种EMT相关蛋白(E-钙黏蛋白、N-钙黏蛋白和波形蛋白)的表达。结果表明,CRC组织样本中YB-1的表达高于配对的正常对照,且与肿瘤分化、肿瘤侵袭、淋巴结转移和远处转移显著相关。此外,分析表明YB-1表达与E-钙黏蛋白呈负相关,与N-钙黏蛋白和波形蛋白表达呈正相关。体外实验表明,敲低YB-1可抑制HT-29 CRC细胞系的增殖、抗凋亡、侵袭和迁移。值得注意的是,敲低YB-1后,E-钙黏蛋白表达升高,而N-钙黏蛋白和波形蛋白表达降低。综上所述,这些结果表明YB-1部分通过诱导EMT促进CRC的恶性进展,因此YB-1可能是CRC治疗的一个潜在新靶点。

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