Abstract
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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-016-2154-z) contains supplementary material, which is available to authorized users.
Highlights
The deregulation of E-cadherin has been considered as a leading cause of hepatocellular carcinoma (HCC) metastasis
In summary, this study shows that the expression of BCL6 corepressor-like 1 (BCORL1) is up-regulated in HCC tissues as compared with that in matched adjacent noncancerous tissues
Clinical association analyses indicate that high expression of BCORL1 is associated with poor prognostic features of HCC
Summary
The deregulation of E-cadherin has been considered as a leading cause of hepatocellular carcinoma (HCC) metastasis. Hepatocellular carcinoma (HCC) is the 5th most frequent malignancy and 3rd most common cause of cancer mortality in the world [1]. Numerous studies have reported that impaired expression and/or dysfunction of E-cadherin leads to loss of epithelial phenotype and promotes cell migration and invasion in human cancer [5]. Loss expression of E-cadherin contributes to epithelialmesenchymal transition (EMT), which is a main cause of tumor metastasis [6]. It has been demonstrated that reduced expression of E-cadherin was correlated with invasion and metastasis of various human cancers including HCC [7]. Transcriptional repressors including Snail, Slug, Twist, Zinc finger E-box-binding homeobox 1/2 (ZEB1/2) and C-terminal-binding protein (CtBP) are involved in the regulation of E-cadherin expression [8, 9]
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