BackgroudAccumulating evidences indicate that circular RNAs (circRNAs), a class of non-coding RNAs, play important roles in tumorigenesis. However, the function of circRNAs in hepatocellular cancer (HCC) is largely unknown.MethodsWe performed circRNA microarrays to identify circRNAs that are aberrantly expressed in HCC tissues. Expression levels of a significantly upregulated circRNA, circFBLIM1, was detected by quantitative real-time PCR (qRT-PCR) in HCC cell lines and tissues. Then, we examined the functions of circFBLIM1 in HCC by cell proliferation, apoptosis, invasion and mouse xenograft assay. In addition, luciferase assay and RNA immunoprecipitation (RIP) assay were used to explore the miRNA sponge function of circFBLIM1 in HCC.ResultsMicroarray analysis and qRT-PCR verified a circRNA termed circFBLIM1 that was upregulated in HCC tissues and cell lines. Knockdown of circFBLIM1 inhibited proliferation, invasion and promoted apoptosis in HCC. Via luciferase reporter assays, circFBLIM1 and FBLIM1 were observed to directly bind to miR-346. Subsequent experiments showed that circFBLIM1 and FBLIM1 regulated the expression of each other by sponging miR-346.ConclusionsTaken together, we conclude that circFBLIM1 may function as a competing endogenous RNA (ceRNA) to regulate FBLIM1 expression through sponging miR-346 to exert regulatory functions in HCC. circFBLIM1 may be a diagnostic biomarker and potential target for HCC therapy.
Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in China. We aimed to first present the expression of endocan in HCC tissue and its correlation with the clinicopathological features and overall survival of patients with HCC after curative hepatectomy. Immunohistochemical detection of endocan, CD34, and vascular endothelial growth factor (VEGF) were performed on samples from 100 patients with HCC. Endocan protein was expressed in endothelium of HCC tissue in all specimens, but was not expressed in endothelium of pericarcinomatous liver tissue and normal liver tissue. Microvessel density (MVD) denoted by endocan (endocan-MVD) in HCC was correlated with microscopic venous invasion and VEGF expression (P < 0.05). Survival analysis showed that overall survival of patients was inversely associated with endocan-MVD (P < 0.01). Multivariate analysis showed that endocan-MVD was an independent prognostic marker for overall survival of HCC (P < 0.01). In conclusion, endocan-MVD was a significant factor to predict the prognosis of HCC patients after curative hepatectomy.
Background Many recent studies have demonstrated the predominant role chronic inflammation plays in cancer cell propagation, angiogenesis and immunosuppression. Cancer-related inflammation (CRI) has been shown to correlate with poor cancer prognosis. Our study aimed to evaluate the prognostic value of the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) in patients with hepatocellular carcinoma (HCC) who have undergone liver resection. Methods Between 2012 and 2015, 239 patients with HCC who had undergone liver resection at XiangYa Hospital Central South University were included in this study. The values of simple inflammatory markers, including the NLR and PLR, used in predicting the long-term outcomes of these patients were evaluated using Kaplan–Meier curves and Cox regression models. Results The cutoff values of the NLR and PLR were 2.92 and 128.1, respectively. In multivariate Cox regression analysis, high NLR (≥2.92) and high PLR (≥128.1) were independent risk factors predicting poorer outcomes in patients with HCC. However, high NLR and high PLR were prognostic factors in tumor size and tumor number. Conclusions In this study, we identified that high NLR (≥2.92) and high PLR (≥128.1) are useful prognostic factors in predicting outcomes in patients with HCC whom underwent liver resection.
Epithelial-mesenchymal transition (EMT) is a critical step in the metastasis of hepatocellular carcinoma (HCC). BTB/POZ domain-containing protein 7 (BTBD7) regulates EMTassociated proteins implicated in HCC progression. However, the role(s) of BTBD7 in HCC have not been identified. Using highly metastatic HCC HCCLM3 cells, immortalized L02 hepatocytes, metastatic HCC animal models, and three independent cohorts of HCC patient specimens, we aimed to determine the involvement of BTBD7 in HCC metastasis. We show that BTBD7 messenger RNA and protein was highly expressed in HCC cells and tumor tissues, with such expression being associated with: enhanced cell motility, venous invasion, and poor prognosis. BTBD7 promoted HCC angiogenesis and metastasis in vitro and in vivo, but did not influence cell proliferation or colony formation. BTBD7 enhancement of HCC invasion and EMT phenotype occurred through activation of a RhoC-Rock2-FAK-signaling pathway, resulting in matrix metalloproteinase-2/9 production and microvessel formation. Applying a predictive risk score model, Cox regression analysis revealed that high BTBD7 expression integrated with high microvessel density was a powerful independent predictive factor of HCC clinical outcome. Conclusion: The present study identifies BTBD7 as a novel candidate prognostic factor and a potential therapeutic target of HCC. (HEPATOLOGY 2013; 57:2326-2337 H epatocellular carcinoma (HCC) is the third leading cause of cancer-related death worldwide. Overall survival (OS) of HCC patients remains unsatisfactory because of a high incidence of recurrence and metastasis after hepatic resection. 1 Understanding the mechanisms of HCC recurrence and metastasis should improve HCC treatment and outcomes.Epithelial-mesenchymal transition (EMT) is an important physiological process contributing to HCC recurrence and metastasis. Expression of several EMTassociated genes is correlated with HCC recurrence and metastasis. HCCs with EMT features consistently exhibit more venous invasion, metastases, and a poorer prognosis than those without EMT characteristics. 2 Therefore, for the treatment of HCC, there exists significant clinical potential in targeting EMT-associated factors.Members of the BTB (bric-a-brac tramtrack broad complex) (also known as POZ) gene family, characterized by a conserved BTB/POZ protein-protein interaction motif, have been implicated in human cancer. 3,4 The promoter region of BTB/POZ domain-containing protein 7 (BTBD7) contains binding sites for notable transcription factors, including alpha-fetoprotein (AFP)-1, CAAT enhancer-binding protein beta, GATA,
Egfl7 is significantly upregulated in human epithelial tumor tissues, suggesting Egfl7 to be a potential biomarker for human epithelial tumors, especially HCC and breast cancer.
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