Hepatic Cell News Volume 3.40 | Oct 25 2019

TOP STORY

The Tumor Suppressor TMEM127 Regulates Insulin Sensitivity in a Tissue-Specific Manner

Liver-specific and adipose-specific Tmem127 deletion partially overlapped global Tmem127 loss: liver Tmem127 promoted hepatic gluconeogenesis and inhibited peripheral glucose uptake, while adipose Tmem127 downregulated adipogenesis and hepatic glucose production. [Nat Commun] Full Article

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miR24-2 Promotes Malignant Progression of Human Liver Cancer Stem Cells by Enhancing Tyrosine Kinase Src Epigenetically

Mechanically, the miR24-2 targeted the 3′-UTR of protein arginine methyltransferase 7 inhibited the translational ability of prmt7 gene. Moreover, miR24-2 inhibited the di-/tri-methylation of histone H4 arginine 3 by reducing PRMT7, and then promoted the expression of Nanog via long noncoding RNA HULC. [Mol Ther] Abstract

CCL14 Serves as a Novel Prognostic Factor and Tumor Suppressor of HCC by Modulating Cell Cycle and Promoting Apoptosis

The authors found for the first time that CCL14 was downregulated in hepatoceullar carcinoma (HCC) tumor tissues compared with peritumor tissues. Meanwhile, CCL14 low expression in HCC tumor tissues was associated with a poor prognosis. CCL14 also displayed its predictive value in high differentiation, liver cirrhosis, and no tumor capsule subgroups. [Cell Death Dis] Full Article

Hepatocarcinoma-Intestine-Pancreas/Pancreatitis-Associated Protein (HIP/PAP) Confers Protection against Hepatic Fibrosis through Downregulation of Transforming Growth Factor β Receptor II

In vitro experiments demonstrated that, in addition to suppressing hepatic stellate cell proliferation and accelerating hepatocyte proliferation, hepatocarcinoma-intestine-pancreas/pancreatitis-associated protein mitigated TGF-β1-induced hepatic stellate cell activation, hepatocyte epithelial-mesenchymal transition and upregulated expression of profibrotic cytokines in both hepatic stellate cells and hepatocytes. [Lab Invest] Abstract

The PNPLA3 I148M Variant Promotes Lipid-Induced Hepatocyte Secretion of CXC Chemokines Establishing a Tumorigenic Milieu

In vitro, lipid stimulation of transduced hepatocytes dose-dependently induced the production of interleukin-8 and CXCL1 in hepatocytes carrying the PNPLA3 148M variant. In line, sera from PNPLA3 148M-positive patients with alcoholic liver cirrhosis contained higher levels of interleukin-8 and CXCL1 than patients with wild-type PNPLA3. [J Mol Med] Abstract

The Protein Kinase CK2 Contributes to the Malignant Phenotype of Cholangiocarcinoma Cells

Investigators used chemical inhibition of CK2 and genetic modification by CRISPR/Cas9 to explore the contribution of CK2 to the malignant phenotype of cholangiocarcinoma cells. Disruption of CK2 activity resulted in cell death through apoptosis, reduced invasion and migration potential, and G0/G1 cell cycle arrest. [Oncogenesis] Full Article

Decellularized Liver Matrix as Substrates for Rescue of Acute Hepatocytes Toxicity

Scientists mixed rat decellularized liver matrix with gelatin-hydroxyphenylpropionic acid to form a three-dimensional structure to simulate the in vivo liver environment, and cultured the primary rat hepatocytes in it. Afterward, the hepatocytes were treated using D-galactosamine, CHCl3, and CCl4-containing medium to simulate the toxin-mediated liver fibrosis in vitro. [J Biomed Mater Res B Appl Biomater] Abstract

Saxagliptin Protects Against Hypoxia-Induced Damage in H9c2 Cells

Researchers used real-time polymerase chain reaction, Western blot analysis, and enzyme linked immunosorbent assay to investigate the effects of saxagliptin on hypoxia-inducible factors. They demonstrated that saxagliptin can significantly improved cell viability in H9c2 cells as well as reduced hypoxia-induced oxidative damage and loss of mitochondrial membrane potential. [Chem Biol Interact] Full Article

ApoE-Modified Liposomes Mediate the Antitumor Effect of Survivin Promoter-Driven HSVtk in Hepatocellular Carcinoma

Apolipoprotein E-modified liposomes were used for targeted gene delivery to the tumor tissue, and the survivin promoter was used to drive thymidine kinase/ganciclovir (HSVtk) expression in hepatoceullar carcinoma cells. Scientists showed that the survivin promoter was specifically activated in tumor cells, and HSVtk was expressed selectively in tumor cells. [Cancer Gene Ther] Abstract

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Acetaminophen-Induced Liver Damage in Hepatic Steatosis

The knowledge about the damage to the liver or APAP in susceptible people like obese and non-alcoholic fatty liver disease (NAFLD) is of great relevance for the sanitary sector since it would imply strategies of different therapeutic approach in such patients. The authors review the role of APAP in liver damage in the presence of obesity, NAFLD, and non-alcoholic steatohepatitis. [Clin Pharmacol Ther] Abstract

Roles of Thyroid Hormone-Associated MicroRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. Investigators discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. [Int J Mol Sci] Abstract

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Genentech’s Tecentriq in Combination with Avastin Increased Overall Survival and Progression-Free Survival in People with Unresectable Hepatocellular Carcinoma

Genentech announced that the Phase III IMbrave150 study, evaluating Tecentriq^®in combination with Avastin^® as a treatment for people with unresectable hepatocellular carcinoma who have not received prior systemic therapy, met both of its co-primary endpoints demonstrating statistically significant and clinically meaningful improvements in overall survival and progression-free survival compared with standard-of-care sorafenib. [Genentech] Press Release

Spanish Government Approves National Reimbursement of ORKAMBI^® (Lumacaftor/Ivacaftor) and SYMKEVI^® (Tezacaftor/Ivacaftor) in Combination With KALYDECO^® (Ivacaftor)

Vertex Pharmaceuticals Incorporated announced that the Spanish Government has approved terms for the national reimbursement of ORKAMBI^® and SYMKEVI^® in combination with KALYDECO^® for eligible patients in Spain living with cystic fibrosis (CF). Under the terms announced, children ages six to 11 years with CF who have two copies of the F508del mutation in the cystic fibrosis transmembrane conductance regulator gene can be treated with ORKAMBI. [Vertex Pharmaceuticals] Press Release

Argentine Scientists Rally Behind Favorite in Sunday’s Presidential Election

Thousands of Argentine scientists are hoping the man expected to be the country’s next president will reverse deep cuts to research imposed by the conservative government of President Mauricio Macri. But the first priority for Alberto Fernández, the front-runner in October 27^th‘s election, will almost certainly be Argentina’s crumbling economy. And it’s not clear when- or how effectively- the concerns of scientists will be addressed. [ScienceMagazine] Editorial

German University Finds ‘Severe’ Misconduct by Researcher Who Promoted Questionable Cancer Blood Test

A university commission announced this week it had found evidence of “extensive and severe scientific misconduct” by Christof Sohn, director of the women’s clinic at Heidelberg University Hospital in Germany and the lead researcher behind a highly publicized but questionable blood test designed to detect breast cancer. [ScienceMagazine] Editorial

Some of NIH’s Chimpanzees Will Not Retire to a Sanctuary as Planned

The US National Institutes of Health (NIH) will not be retiring all of its chimpanzees to a sanctuary, as it originally pledged to do, agency head Francis Collins announced. Nearly four dozen chimps at a biomedical primate facility in New Mexico will remain there because they are too old and sick to move, he said, although scientific studies of them have ended. [ScienceMagazine] Editorial

NEW Islet Biology: From Gene to Cell to Micro-Organ
January 27-31, 2020
Santa Fe, New Mexico, United States

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NEW Postdoctoral Researcher – Liver Plasticity (University of Southern Denmark)

Postdoctoral Scientist – RAS Cancer Biology (Genetech, Inc.)

Postdoctoral Associates – Organogenesis of Liver, Heart and Pancreas (The University of Manchester)

Assistant Professor – Liver Research (The University of Hong Kong)

Research Associate – Pluripotent Stem Cells in Liver Development (The Wellcome Institute)

Postdoctoral Researcher – Gene Regulation in Liver Cancer (Umeå University)

Research Scientist – Fibrosis (Gilead Sciences, Inc.)

Postdoctoral Researcher – Liver Cell-Cell Interactions (Flanders Institute for Biotechnology)

Postdoctoral Researcher – Liver Disease (Albert Einstein College of Medicine)

Principal Researcher – Systems Disease Biology (Boehringer Ingelheim)

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