A5056794040- Cancer, Lipids, and Metabolism
- Cancer, Hypoxia, and Metabolism
- Peroxisome Proliferator-Activated Receptors
- Lipid metabolism and biosynthesis
- RNA modifications and cancer
- Endoplasmic Reticulum Stress and Disease
- Hippo pathway signaling and YAP/TAZ
- Cholangiocarcinoma and Gallbladder Cancer Studies
- RNA Research and Splicing
- Heat shock proteins research
- DNA Repair Mechanisms
- Ubiquitin and proteasome pathways
- PI3K/AKT/mTOR signaling in cancer
- Cancer Mechanisms and Therapy
- Diet and metabolism studies
- ATP Synthase and ATPases Research
- Computational Drug Discovery Methods
- Genomics, phytochemicals, and oxidative stress
- Peptidase Inhibition and Analysis
- Biochemical and Molecular Research
- Metabolism, Diabetes, and Cancer
- Genomics and Chromatin Dynamics
- Liver physiology and pathology
- Amino Acid Enzymes and Metabolism
- Cancer Research and Treatments
University of Sassari
2012-2018
Abstract Activation of the AKT/mTOR cascade and overexpression c-Met have been implicated in development human hepatocellular carcinoma (HCC). To elucidate functional crosstalk between two pathways, we generated a model characterized by combined expression activated AKT mouse liver. Co-expression triggered rapid liver tumor mice required to be euthanized within 8 weeks after hydrodynamic injection. At molecular level, tumors induced AKT/c-Met display activation Ras/MAPK cascades as well...
Hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) are the most prevalent types of primary liver cancer. These malignancies have limited treatment options, resulting in poor patient outcomes. Metabolism reprogramming, including increased de novo lipogenesis, is one hallmarks Fatty acid synthase (FASN) catalyzes synthesis long‐chain fatty acids from acetyl‐coenzyme A malonyl‐coenzyme A. Increased FASN expression has been reported multiple tumor types, inhibition shown to...
Down-regulation of the liver-specific MAT1A gene, encoding S-adenosylmethionine (SAM) synthesizing isozymes MATI/III, and up-regulation widely expressed MAT2A , MATII isozyme, known as MAT1A:MAT2A switch, occurs in hepatocellular carcinoma (HCC). Here we found Mat1A:Mat2A switch low SAM levels, associated with CpG hypermethylation histone H4 deacetylation Mat1A promoter, prevalent hypomethylation acetylation Mat2A promoter fast-growing HCC F344 rats, genetically susceptible to...
Hepatocellular carcinoma (HCC), the most frequent primary tumor of liver, is an aggressive cancer type with limited treatment options. Cumulating evidence underlines a crucial role aberrant lipid biosynthesis (a process known as de novo lipogenesis) along carcinogenesis. Previous studies showed that suppression fatty acid synthase (FASN), major enzyme responsible for lipogenesis, highly detrimental in vitro growth HCC cell lines. To assess whether lipogenesis required liver carcinogenesis,...
The DNA-repair gene DNA-dependent kinase catalytic subunit (DNA-PKcs) favours or inhibits carcinogenesis, depending on the cancer type. Its role in human hepatocellular carcinoma (HCC) is unknown.DNA-dependent protein subunit, H2A histone family member X (H2AFX) and heat shock transcription factor-1 (HSF1) levels were assessed by immunohistochemistry and/or immunoblotting qRT-PCR a collection of HCC. Rates proliferation, apoptosis, microvessel density genomic instability also determined....
Activating mutations of PIK3CA occur in various tumour types, including human hepatocellular carcinoma. The mechanisms whereby contributes to hepatocarcinogenesis remain poorly understood.PIK3CA mutants H1047R or E545K were hydrodynamically transfected, either alone combination with NRasV12 c-Met genes, the mouse liver.Overexpression was able induce AKT/mTOR signalling liver, leading hepatic steatosis. However, none mice developed liver tumours over long term. In contrast, cooperated rapidly...
Upregulation of the heat shock transcription factor 1 (HSF1) has been described as a frequent event in many cancer types, but its oncogenic role hepatocellular carcinoma (HCC) remains poorly delineated. In present study, we assessed function(s) HSF1 hepatocarcinogenesis via vitro and vivo approaches. particular, determined importance on v-Akt murine thymoma viral oncogene homolog (AKT)-induced liver development mice. We found that knockdown activity specific siRNA triggered growth restraint...
// Maria M. Simile 1, * , Gavinella Latte I. Demartis 1 Stefania Brozzetti 2 Diego F. Calvisi Alberto Porcu 3 Claudio Feo A. Seddaiu Lucia Daino Carmen Berasain 4, 5, 6 L. Tomasi 7, 8 Matias Avila Francesco Rosa Pascale Department of Clinical and Experimental Medicine, Division Pathology Oncology, University Sassari, Italy Surgery ''Pietro Valdoni'', Rome 'Sapienza'', Rome, Surgery, 4 Hepatology, Centro de Investigación Médica Aplicada (CIMA), Navarra, Pamplona, Spain 5 CIBERehd, Instituto...
// Antonio Cigliano 1,* , Maria G. Pilo 2,* Lei Li 3,* Gavinella Latte 2 Marta Szydlowska 1 M. Simile Panagiotis Paliogiannis Che 4 Giovanni Pes Giuseppe Palmieri 5 C. Sini Cossu 6 Alberto Porcu Gianpaolo Vidili A. Seddaiu Rosa Pascale Silvia Ribback Frank Dombrowski Xin Chen and Diego F. Calvisi Institut für Pathologie, Universitätsmedizin Greifswald, Germany Department of Clinical Experimental Medicine, University Sassari, Italy 3 School Pharmacy, Tongji Medical College, Huazhong...
Metabolic reprogramming is a hallmark of many cancer types, including hepatocellular carcinoma (HCC). Identifying the critical players in this process might be crucial for generation novel and effective anti-neoplastic therapies. In present investigation, we determined importance carbohydrate responsive element binding protein (ChREBP), central player regulation lipid glucose metabolism liver, on development HCC vitro vivo models. We found that genetic deletion ChREBP (that will referred to...
The proteins of MAF family (the cellular counterpart viral oncogene MAF, isolated from avian musculoaponeurotic fibrosarcoma) are transcription factors regulating gene expression. On the bases size, they sub-grouped into two families: "large" (L-MAFs: MAFA, MAFB, c-MAF, and Nrl) "small" (S-MAFs: MAFF, MAFK, MAFG) (1).
Cholangiocarcinoma (CCA) is a highly malignant tumor and the second-most common primary liver cancer. Chronic inflammation cholestasis predispose to CCA. Previous work showed role of c-MYC upregulation in cholestatic injury (1), during CCA progression using murine model cholestasis-associated (2).
PIK3CA, encoding the catalytic subunit p110α of class I phosphoinositide-3-kinase (PI3K), is mutated or overexpressed in many tumors, including hepatocellular carcinoma (HCC), where it supposed to act as an oncogene. Here, we developed new mouse models investigate oncogenic effects gain-of-function PIK3CA mutations and identified downstream PI3K signaling components liver.