AimTo investigate the expression and clinical significance of Holliday junction–recognizing protein (HJURP) in hepatocellular carcinoma (HCC).MethodsIn this study, we detected the expression of HJURP protein in samples of 164 patients with HCC, and based on this, we divided the patients into two cohorts: high expression of HJURP and low expression of HJURP. We analyzed the correlation between HJURP expression and the clinicopathological factors using chi-square test. Survival significance of HJURP was defined by Kaplan–Meier method and log-rank test, and the independent prognostic factors were identified by Cox regression model. Using function assays of HCC cell lines, we investigated the influence of HJURP on the proliferation of HCC cells.ResultsIn our study, the proportion of patients with high HJURP expression was 25.6%, which was significantly associated with the tumor size and Barcelona clinic liver cancer stage. Univariate analysis confirmed that high HJURP expression was remarkably associated with poorer overall survival rates (P=0.003), as well as tumor number (P=0.016), tumor differentiation (P=0.047), TNM stage (P=0.005), and Barcelona clinic liver cancer stage (P=0.004). Multivariate analysis confirmed that high HJURP expression (P<0.001) acted as an independent prognostic risk factor of unfavorable prognosis. Real-time polymerase chain reaction analysis revealed that the expression of HJURP was significantly higher in HCC tissues than that in the corresponding normal liver tissues. Moreover, we demonstrated that HJURP overexpression could accelerate HCC cell line proliferation, whereas HJURP knockdown could attenuate the proliferation.ConclusionHigh HJURP expression was an independent prognostic biomarker of HCC, predicting poorer prognosis. HJURP also played an important role in HCC cell proliferation.

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In the present study, mitral valve tissues from three mitral stenosis patients with RHD by valve replacement and two healthy donors were harvested and conducted DNA methylation signature on PRKCA by MeDIP-qPCR. The presence of hypomethylated CpG islands at promoter and 5ʹ terminal of PRKCA was observed in RHD accompanied with highly expressed PRKCA and downregulated antisense long non-coding RNA (lncRNA) PRKCA-AS1 compared to health control. Furthermore, the enrichments of DNMT1/3A/3B on PRKCA were detected by ChIP-qPCR assay in vivo and in human cardiomyocyte AC16 and RL-14 cells exposed to TNF-α in vitro, and both demonstrated that DNMT1 substantially contributed to DNA methylation. Additionally, PRKCA-AS1 was further determined to bind with promoter of PRKCA via 5ʹ terminal and interact with DNMT1 via 3ʹ terminal. Taken together, our results illuminated a novel regulatory mechanism of DNA methylation on regulating PRKCA transcription through lncRNA PRKCA-AS1, and shed light on the molecular pathogenesis of RHD occurrence.