BCORL1 is an independent prognostic marker and contributes to cell migration and invasion in human hepatocellular carcinoma

BMC Cancer

Research Article

Qingguang Liu¹  Yufeng Wang¹  Changwei Dou¹  Guozhi Yin¹  Zhikui Liu¹  Chao Li¹  Yingmin Yao¹  Kangsheng Tu¹  Wei Yang¹ 

[1] Department of Hepatobiliary Surgery, the First Affiliated Hospital of Xi’an Jiaotong University, No.277 Yanta West Road, 710061, Xi’an, China;

关键词: BCL6 corepressor-like 1;    Hepatocellular carcinoma;    Prognostic marker;    E-cadherin;    Tumor metastasis;   

DOI  :  10.1186/s12885-016-2154-z

 received in 2015-06-21, accepted in 2016-02-10,  发布年份 2016

来源: Springer

【 摘 要 】

BackgroundThe deregulation of E-cadherin has been considered as a leading cause of hepatocellular carcinoma (HCC) metastasis. BCL6 corepressor-like 1 (BCORL1) is a transcriptional corepressor and contributes to the repression of E-cadherin. However, the clinical significance of BCORL1 and its role in the metastasis of HCC remain unknown.MethodsDifferentially expressed BCORL1 between HCC and matched tumor-adjacent tissues, HCC cell lines and normal hepatic cell line were detected by Western blot. The expression of BCORL1 was altered by siRNAs or lentivirus-mediated vectors. Transwell assays were performed to determine HCC cell invasion and migration.ResultsIncreased expression of BCORL1 protein was detected in HCC specimens and cell lines. Clinical association analysis showed that BCORL1 protein was expressed at significant higher levels in HCC patients with multiple tumor nodes, venous infiltration and advanced TNM tumor stage. Survival analysis indicated that high expression of BCORL1 protein conferred shorter overall survival (OS) and recurrence-free survival (RFS) of HCC patients. Multivariate Cox regression analysis disclosed that BCORL1 expression was an independent prognostic marker for predicting survival of HCC patients. Our in vitro studies demonstrated that BCORL1 prominently promoted HCC cell migration and invasion. Otherwise, an inverse correlation between BCORL1 and E-cadherin expression was observed in HCC tissues. BCORL1 inversely regulated E-cadherin abundance and subsequently facilitated epithelial-mesenchymal transition (EMT) in HCC cells. Notably, the effect of BCORL1 knockdown on HCC cells was abrogated by E-cadherin silencing.ConclusionsBCORL1 may be a novel prognostic factor and promotes cell migration and invasion through E-cadherin repression-induced EMT in HCC.

【 授权许可】

CC BY   
© Yin et al. 2016