Torin2 overcomes sorafenib resistance via suppressing mTORC2-AKT-BAD pathway in hepatocellular carcinoma cells.

Background: Sorafenib is an oral multi-kinase inhibitor that was approved by the US Food and Drug Administration for the treatment of patients with advanced hepatocellular carcinoma (HCC). However, resistance to sorafenib is an urgent problem to be resolved to improve the therapeutic efficacy of sorafenib. As the activation of AKT/mTOR played a pivotal role in sorafenib resistance, we evaluated the effect of a dual mTOR complex 1/2 inhibitor Torin2 on overcoming the sorafenib resistance in HCC cells.

Impact of treatment modalities on patients with recurrent hepatocellular carcinoma after liver transplantation: Preliminary experience.

Background: Post-liver transplantation (LT) hepatocellular carcinoma (HCC) recurrence still occurs in approximately 20% of patients and drastically affects their survival. This study aimed to evaluate the efficacy of various treatments for recurrent HCC after LT in a Chinese population.

Methods: A total of 64 HCC patients with tumor recurrence after LT were enrolled in this study.

Multidisciplinary Treatment of Advanced Hepatocellular Carcinoma.

Current strategy for treatment of hepatocellular carcinoma (HCC) based on Barcelona-Clinic Liver Cancer (BCLC) criteria dictates that patients with advanced-stage HCC are to only receive treatment with tyrosine kinase inhibitors. However, they prolong overall survival just by slightly more than 6 months. In this article, we present a patient with HCC diagnosed at an advanced stage who received multidisciplinary treatment consisting of transarterial chemoembolization, hepatic resection, pulmonary resection, radiofrequency ablation, tyrosine kinase inhibitors, and radiotherapy, and has survived for more than 2 years since diagnosis and counting.

Kupffer cells contribute to concanavalin A-induced hepatic injury through a Th1 but not Th17 type response-dependent pathway in mice.

Background: Increasing evidence suggests that a close interaction of Kupffer cells with T cells plays a central role in concanavalin A-induced hepatic injury in mice, but the underlying mechanisms remain obscure. The present study aimed to determine the relative roles of Th1 and Th17 type responses in concanavalin A-induced hepatic injury in mice, and to investigate whether or not Kupffer cells contribute to hepatic injury via a Th1 or Th17 type response-dependent pathway.

Methods: Immune-mediated hepatic injury was induced in C57BL/6 mice by intravenous injection of concanavalin A.

Th17 promotes acute rejection following liver transplantation in rats.

T help cell 17 (Th17), recently identified as a new subset of CD4(+) T cells, has been implicated in autoimmune diseases, tumor immunity, and transplant rejection. To investigate the role of Th17 in acute hepatic rejection, a rat model of allogeneic liver transplantation (Dark Agouti (DA) to Brown Norway (BN)) was established and isogeneic liver transplantation (BN to BN) was used as controls in the study. The expression of Th17-related cytokines in the liver and peripheral blood was determined by immunohistochemistry, flow cytometry, enzyme-linked immunosorbent assay (ELISA), or real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR).

The impact of miR-34a on protein output in hepatocellular carcinoma HepG2 cells.

MicroRNAs are small non-coding RNA molecules that play essential roles in biological processes ranging from cell cycle to cell migration and invasion. Accumulating evidence suggests that miR-34a, as a key mediator of p53 tumor suppression, is aberrantly expressed in human cancers. In the present study, we aimed to explore the precise biological role of miR-34a and the global protein changes in HCC cell line HepG2 cells transiently transfected with miR-34a.