A5032169892- Circadian rhythm and melatonin
- Genomics, phytochemicals, and oxidative stress
- Diet, Metabolism, and Disease
- Hepatocellular Carcinoma Treatment and Prognosis
- Protein Tyrosine Phosphatases
- RNA modifications and cancer
- Glutathione Transferases and Polymorphisms
- Cancer, Hypoxia, and Metabolism
- Liver Disease Diagnosis and Treatment
- Ferroptosis and cancer prognosis
- Cancer, Lipids, and Metabolism
- Immunotherapy and Immune Responses
- Cancer Cells and Metastasis
- Liver physiology and pathology
- Cancer Immunotherapy and Biomarkers
- Angiogenesis and VEGF in Cancer
- PI3K/AKT/mTOR signaling in cancer
- Endoplasmic Reticulum Stress and Disease
- RNA Research and Splicing
University of California, San Diego
2015-2024
Moores Cancer Center
2020-2024
The mechanisms of Myc-driven liver tumorigenesis are inadequately understood. Herein we show that hepatocellular carcinoma (HCC) is dramatically aggravated in mice with hepatocyte-specific Ptpn11/Shp2 deletion. However, Myc-induced tumors develop selectively from the rare Shp2-positive hepatocytes Shp2-deficent liver, and oncogenesis depends on an intact Ras-Erk signaling promoted by Shp2 to sustain Myc stability. Despite a stringent requirement cell autonomously, deletion induces...
The complexity of liver tumorigenesis is underscored by the recently observed anti-oncogenic effects oncoproteins, although mechanisms are unclear. Shp2/Ptpn11 a proto-oncogene in hematopoietic cells and antagonizes effect tumor suppressor Pten leukemogenesis. In contrast, we show here cooperative functions Shp2 suppressing hepatocarcinogenesis. Ablating both hepatocytes induced early-onset non-alcoholic steatohepatitis (NASH) promoted genesis tumor-initiating likely due to augmented cJun...
The chemical carcinogen diethylnitrosamine (DEN) is often used to induce HCC in mice. Curiously, several labs have reported that the removal of oncoproteins from hepatocytes exacerbated DEN-induced HCC, with mechanisms unknown. This study aimed at deciphering molecular underlying tumor suppressive effect oncoproteins.
The Ras/Erk and NF-κB pathways play critical roles in cell proliferation are known to drive oncogenesis when overactivated. Herein we report a gatekeeper function of the two by working synergy suppress liver tumorigenesis. Hepatocyte-specific deletion both Shp2/Ptpn11 Ikkβ mice, which promote signaling, respectively, exacerbated chemical carcinogenesis even triggered spontaneous development hepatocellular carcinoma (HCC). We show that unanticipated severe tumor phenotype was contributed...
<div>Abstract<p>The Ras/Erk and NF-κB pathways play critical roles in cell proliferation are known to drive oncogenesis when overactivated. Herein we report a gatekeeper function of the two by working synergy suppress liver tumorigenesis. Hepatocyte-specific deletion both Shp2/Ptpn11 Ikkβ mice, which promote signaling, respectively, exacerbated chemical carcinogenesis even triggered spontaneous development hepatocellular carcinoma (HCC). We show that unanticipated severe tumor...
SupplementaryFigure from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
<div>Abstract<p>The Ras/Erk and NF-κB pathways play critical roles in cell proliferation are known to drive oncogenesis when overactivated. Herein we report a gatekeeper function of the two by working synergy suppress liver tumorigenesis. Hepatocyte-specific deletion both Shp2/Ptpn11 Ikkβ mice, which promote signaling, respectively, exacerbated chemical carcinogenesis even triggered spontaneous development hepatocellular carcinoma (HCC). We show that unanticipated severe tumor...
SupplementaryFigure from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis
Supplementary Data from Concurrent Disruption of the Ras/MAPK and NF-κB Pathways Induces Circadian Deregulation Hepatocarcinogenesis