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liver ischemia-reperfusion (i/r) injury is an important clinical issue related to liver transplantation. recent studies suggest that micrornas are implicated in various biological and pathological processes, including liver i/r injury. This study aimed to investigate the role and potential mechanism of mir-27a during liver i/r injury. a liver i/r model was induced via 60 min of ischemia and reperfusion for 6 h in rats. cells were transfected with mir-27a mimics or the mir-27a inhibitor to examine the effect of mir-27a on liver i/r. apoptotic cells were detected by flow cytometry and TUNEL staining. The expression of mir-27a was measured by real-time Pcr. The expression of peroxisome proliferator-activated receptor γ (PParγ); gastrin-releasing peptide 78 (GrP78) and c/eBP homologous protein (cHoP) were detected by western blot analysis. The results showed that miR-27a was significantly upregulated during i/r injury in vivo and in vitro. in addition, mir-27a inhibitors attenuated hypoxia/reoxygenation (H/r)-induced oxidative stress, endoplasmic reticulum stress (erS) and apoptosis in aMl12 cells. By contrast, mir-27a mimics promoted hypoxia/reoxygenation-induced erS, and apoptosis. Furthermore, PParγ was identified as a target gene of mir-27a using bioinformatic analysis and a dual-luciferase reporter assay. Knockdown of PParγ significantly abrogated the inhibitory effect of mir-27a inhibitors on the erS pathway. Moreover, the mir-27a antagomir attenuated liver i/r injury in rats, a finding manifested by reduced ALT/aST, hepatocyte apoptosis, oxidative stress and inhibition of the erS pathway. Taken together, these findings demonstrate that suppression of mir-27a protects against liver i/r injury by targeting PParγ and by inhibiting the erS pathway.

Increasing evidence has displayed the vital influence of lncRNA in tumorigenesis and chemoresistance of cancer treatment. This study investigated the function of lncRNA PTOV1‐AS1 in hepatocellular carcinoma (HCC) and its role in sorafenib resistance. The relative expression of lncRNA and miRNA was measured by RT‐qPCR. The cellular activities including cell proliferation and invasion were explored by CCK‐8 and Transwell assays. Bioinformatics analysis and dual‐luciferase reporter assay were used to predict the targeting miRNA of PTOV1‐AS1. The expression levels of PTOV1‐AS1 were higher in HCC tissues than that in the normal tissues and associated with patients' overall survival. Knockdown of PTOV1‐AS1 decreased cell proliferation rate and invasion number. After treatment with different concentrations of sorafenib, the sorafenib‐resistant hepatoma cells were conducted. PTOV1‐AS1 expression levels were increased in HepG2‐SR and Huh7‐SR cells. PTOV1‐AS1 knockdown repressed the proliferation, invasion, and drug resistance of sorafenib‐resistant HCC cells by targeting the expression of miR‐505. In conclusion, the expression of PTOV1‐AS1 is increased in HCC and sorafenib‐resistance HCC cells, as well as is associated with patients' prognosis. Inhibition of PTOV1‐AS1 expression can reduce the resistance of sorafenib‐resistant HCC cells, which may play a role by targeting the negative regulation of miR‐505 expression.

As powerful regulatory factors, microRNAs (miRNAs) are involved in tumor progression. The current research aimed to excavate the prognostic significance and potential regulatory mechanisms of miR-652-3p in hepatocellular carcinoma (HCC). Expression of miR-652-3p in HCC tissues and cells was exposed by Quantitative real-time polymerase chain reaction (RT-qPCR) assay, and we found that miR-652-3p was elevated in HCC tissues and cells than in the control group (P < 0.05). Then, the relationship between miR-652-3p levels and clinical characteristics was obtained from the Chi-square test. Kaplan-Meier survival analysis and Cox regression model to explore the outcome of miR-652-3p on the prognosis of HCC. The results investigated that overexpression of miR-652-3p was related to clinical tumor-node-metastasis (TNM) stage (P = 0.020) and differentiation (P = 0.031). HCC patients with elevated miR-652-3p levels were correlated with poor overall survival (log-rank, P = 0.007), and maybe a possible prognostic marker for HCC. Finally, CCK-8, colony formation, wound healing and Transwell assay was detected after transfection of HCC cells with miR-652-3p mimic or inhibitor. And the results confirmed that elevation miR-652-3p promoted the proliferation, migration, and invasion of tumor cells (P < 0.05). All data indicated that elevated miR-652-3p is a prognostic marker and would be able to participate in tumor progression of HCC by regulating cell proliferation, migration, and invasion.

Aim: This study aimed to investigate the expression of microRNA-505 (miR-505) and explore its clinical significance, biological function and mechanisms in hepatocellular carcinoma (HCC). Methods: Expression of miR-505 was measured in 128 paired HCC tissues and five cell lines by quantitative real-time polymerase chain reaction (qRT-PCR). MTT assay, Transwell migration, invasion assays and apoptosis assay were performed to explore the functional role of miR-505. The target gene of miR-505 was assessed using the bioinformatics assay and the related signaling pathway was confirmed using western blot. Results: Expression of miR-505 in HCC serum and tissues were downregulated. The overexpression of miR-505 in HCC cells inhibited cell proliferation and metastasis, as well as enhanced cell apoptosis by directly downregulating heterogeneous nuclear ribonucleoprotein M ( HNRNPM). The activity of the Wnt/β-catenin signaling pathway was suppressed by the overexpression of miR-505 but was promoted by the upregulation of HNRNPM. Conclusion: The results suggest that the regulation of miR-505/ HNRNPM may be a novel strategy to improve the targeted therapy of HCC.