Abstract
Ring finger protein 187 (RNF187) has been identified to be a co-activator linking c Jun to Ras signaling. However, the expression and function of RNF187 in hepatocellular carcinomas (HCC) remains unclear. Here, we tried to determine the expression and roles of RNF187 in hepatocellular carcinomas (HCC).The expression of RNF187 was determined in HCC tissues and cell lines, and we found that RNF187 expressed highly in HCC tissues compared with the corresponding adjacent liver tissues both in mRNA and protein level, which was consistent with the result of immunohistochemistry on HCC tissue microarrays. In HCC cell lines, the level of RNF187 was positively associated with the HCC cells metastatic potential. By the RNF187 interference and cDNA transfection, we showed that the high level of RNF187 induced the HCC cells invasion and metastasis both in vitro and in vivo, as well as the high ability of colony formation.Mechanistically, we detected the high level of RNF187 promoted cell scatter by inducing epithelial-mesenchymal transition (EMT). Clinically, the high level of RNA187 was significantly correlated with a malignant phenotype, including larger tumor size, multiple tumors, and microvascular invasion. Importantly, high level of RNF187 correlated with HCC patients' shorter OS and lower disease free survival rates than those with low level of RNF187. Our results revealed that elevated expression of RNF187 induced hepatocellular carcinoma cell epithelial to mesenchymal transitions, and represented a novel marker for predicting the poor prognosis of HCC.
Highlights
Hepatocellular carcinoma (HCC) is the fifth commonest malignancy and the third leading cause of cancer-related deaths in the world [1]
We tried to determine the expression and roles of Ring finger protein 187 (RNF187) in hepatocellular carcinomas (HCC).The expression of RNF187 was determined in HCC tissues and cell lines, and we found that RNF187 expressed highly in HCC tissues compared with the corresponding adjacent liver tissues both in mRNA and protein level, which was consistent with the result of immunohistochemistry on HCC tissue microarrays
By the RNF187 interference and Complementary DNA (cDNA) transfection, we showed that the high level of RNF187 induced the HCC cells invasion and metastasis both in vitro and in vivo, as well as the high ability of colony formation.Mechanistically, we detected the high level of RNF187 promoted cell scatter by inducing epithelial-mesenchymal transition (EMT)
Summary
Hepatocellular carcinoma (HCC) is the fifth commonest malignancy and the third leading cause of cancer-related deaths in the world [1]. A plethora of studies delineated the important role of EMT in pathogenesis of metastasis in epithelial tumors [7]. Of note is that several new studies have further demonstrated that cancer cells undergoing EMT appeared to gain the ability to resist apoptosis, chemotherapy and immunotherapy, respectively and acquire stem cell features [11,12,13], which further emphasizes the role of EMT in mediating cancer metastasis, and the value of uncovering the fundamental molecular mechanisms underlying EMT. The overexpression of ubiquitin ligase E3C promoted HCC progression by regulating tumor cell EMT [16], and a level of ubiquitin-specific protease 7 accelerated p14ARF degradation by deubiquitinating thyroid hormone receptorinteracting protein 12 and promoting HCC progression [17]. The clinical significance of RNF187 expression was further analyzed using tissue microarray (TMA) in 209 patients with HCC
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