Choibrun7199

These effects were also accompanied by inhibition of cell migration and invasion, indicating that miR-16 can have a significant role as liver cancer suppressor after zingiberene treatment. #link# Luciferase reporter assay confirmed that miR-16, which was one of HCC downregulated miRs, directly targeted Cyclin B1 in HCC cells.

The current study indicates miR-16/cyclin B1 axis might have significant applications as a therapeutic target for patients with liver cancer.

The current study indicates miR-16/cyclin B1 axis might have significant applications as a therapeutic target for patients with liver cancer.

After failure of the first-line sorafenib treatment in advanced or metastatic stage hepatocellular carcinoma (HCC), regorafenib is one of the newly-approved targeted agents. We aimed to evaluate the efficacy of regorafenib in patients with advanced HCC treated in the second- or third-line setting.

In this retrospective and multicenter study, advanced HCC patients not eligible for local therapies, who received a second- or third-line regorafenib therapy after progression on the first-line sorafenib or sequential therapy with chemotherapy (CT) followed by sorafenib, were included.

In the first-line setting, 28 (28.9%) patients received CT and 69 (71.1%) patients received sorafenib. There were 24 (24.7%) patients who were intolerant to sorafenib. Disease control rate (DCR) was 53.6% for all patients treated with regorafenib, 62.3% in patients who received regorafenib in the second-line, and 32.1% for those receiving regorafenib in the third-line (p=0.007). Median progression-free survival (PFS) and overall survival (OS) were 5.6 (range; 4.3-6.9) and 8.8 (range, 6.3-11.3) months for all patients treated with regorafenib vs. 7.1 months and 10.3 months for patients who received regorafenib in the second-line vs. 5.1 and 8.7 months for patients who received regorafenib in the third-line, respectively; however, there was no statistically significant difference (pPFS=0.22 and pOS=0.85).

Although receiving CT as a first-line therapy in advanced HCC patients did not affect the survival rates of subsequent regorafenib therapy, it might diminish the DCR of regorafenib.

Although receiving CT as a first-line therapy in advanced HCC patients did not affect the survival rates of subsequent regorafenib therapy, it might diminish the DCR of regorafenib.

To explore the expression of WD-40 repeat and SOCS box containing 1 (WSB1) and its clinical significance in hepatocellular carcinoma (HCC).

Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of WSB1 in clinical tissues. Survival curves were platted using the Kaplan-Meier method and log rank test was used to compare survival between groups. The influencing factors for the long-term survival were analysed using Cox univariate and multivariate analysis. In in vitro study, Western blot was used to evaluate the effects of WSB1 on epithelial-mesenchymal transition (EMT) of tumor cells.

The expression of WSB1 was much higher in cancer tissues than that in para-normal tissues, and the WSB1 expression was correlated with tumor differentiation, lymph node metastasis and clinical stage. In addition, HCC patients with higher WSB1 expression had significantly poorer progression-free survival (PFS) and overall survival (OS). Both univariate analysis and multivariate analyses indicated that high expression of WSB1 was an independent predictor of poor prognosis in HCC. Further in in vitro study, downregulation of WSB1 in HCC cell line could reduce the expression of epithelial phenotype protein (E-cadherin) while increase the expression of mesenchymal phenotype protein (N-cadherin and Vimentin).

WSB1 might contribute into the development of HCC and serve as a clinical biomarker and a therapeutic target for HCC patients.

WSB1 might contribute into the development of HCC and serve as a clinical biomarker and a therapeutic target for HCC patients.

To explore the influence of transcatheter hepatic arterial chemoembolization (TACE) combined with microwave ablation on T lymphocyte subsets and prognosis in patients with liver cancer and analyze the safety.

The clinical data of 160 patients were retrospectively analyzed. The patients in the control group underwent TACE, while those in the observation group were treated with microwave ablation in addition to TACE. Then, UNC2250 supplier in the levels of T lymphocyte subsets, liver function indexes and alpha-fetoprotein (AFP) before and after treatment were compared between the two groups.

After treatment, the levels of cluster of differentiation 3+ (CD3+), CD4+ and CD4+/CD8+ of patients were significantly increased in both groups, while the levels of CD8+ and serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and AFP were overtly lowered, while the observation group had more obvious changes in the above-mentioned levels (p<0.05). The response rate and prognostic survival rate were evidently higher in the observation group than in the control group (p<0.05). The complications after treatment showed no significant difference between the two groups (p>0.05). Child-Pugh, tumor diameter and number of lesions were independent risk factors for the prognosis of survival of liver cancer patients undergoing TACE combined with microwave ablation (p<0.05).

TACE combined with microwave ablation has relatively high efficacy and safety in the treatment of liver cancer, which can improve liver function, immune function and prognostic survival.

TACE combined with microwave ablation has relatively high efficacy and safety in the treatment of liver cancer, which can improve liver function, immune function and prognostic survival.

This study was set out to explore the role of MAPK activity in programmed cell death ligand-1 (PD-L1) expression in hepatocellular carcinoma (HCC) cells.

The protein expression of PD-L1 was determined by immunofluorescence and immunohistochemistry, and the expression levels of PD-L1 and MAPK-related proteins were determined by flow cytometry and Western blotting. Meanwhile, the RNA transcription level of CD274 was determined by qRT-PCR.

Interferon-γ (IFN-γ), epidermal growth factor receptor (EGFR) and mitogen-activated protein kinase (MAPK) signaling pathways were associated with CD274 gene expression in HCC. Epidermal growth factor (EGF) or IFN-γ stimulation increased CD274 mRNA and PD-L1 protein levels in a representative HCC cell line group, further enhanced by EGF and IFN-γ stimulation. Inhibition of the MAPK pathway by EGFR inhibitors ositinib or MEK 1 and 2 inhibitors selumetinib prevented the up-regulation of CD274 mRNA and PD-L1 proteins and membranes induced by EGF and IFN-γ. IFN-γ increased the transcriptional activity of CD274, while MAPK signaling enhanced the stability of CD274 mRNA.