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| http://dx.doi.org/10.18632/oncoscience.76 | DOI Listing |
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ABCA1 promote tumor environment heterogeneity via epithelial mesenchymal transition in Huh7 and HepG2 liver cancer cell.
Front Pharmacol
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Department of Hepatobiliary Pancreatic Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
In this study, we delve into the intrinsic mechanisms of cell communication in hepatocellular carcinoma (HCC). Initially, employing single-cell sequencing, we analyze multiple malignant cell subpopulations and cancer-associated fibroblast (CAF) subpopulations, revealing their interplay through receptor-ligand interactions, with a particular focus on SPP1. Subsequently, employing unsupervised clustering analysis, we delineate two clusters, C1 and C2, and compare their infiltration characteristics using various tools and metrics, uncovering heightened cytotoxicity and overall invasion abundance in C1.
View Article and Find Full Text PDFHBV-Induced Carcinogenesis: Mechanisms, Correlation With Viral Suppression, and Implications for Treatment.
Liver Int
January 2025
NYU Langone Health, New York, New York, USA.
Background: Chronic hepatitis B virus (HBV) infection is a common but underdiagnosed and undertreated health condition and is the leading cause of hepatocellular carcinoma (HCC) worldwide. HBV (rated a Grade 1 carcinogen by the International Agency for Research on Cancer) drives the transformation of hepatocytes in multiple ways by inducing viral DNA integrations, genetic dysregulation, chromosomal translocations, chronic inflammation, and oncogenic pathways facilitated by some HBV proteins. Importantly, these mechanisms are active throughout all phases of HBV infection.
View Article and Find Full Text PDFThe PRL2 Phosphatase Upregulates miR-21 through Activation of the JAK2/STAT3 Pathway to Downregulate the PTEN Tumor Suppressor.
Biochem J
December 2024
Purdue University, West Lafayette, Indiana, United States.
The Phosphatases of Regenerating Liver (PRLs) are members of the protein tyrosine phosphatase (PTP) superfamily that play pro-oncogenic roles in cell proliferation, migration, and survival. We previously demonstrated that PRLs can post-translationally downregulate PTEN, a tumor suppressor frequently inactivated in human cancers, by dephosphorylating PTEN at Tyr336, which promotes the NEDD4-mediated PTEN ubiquitination and proteasomal degradation. Here we report that PRLs can also reduce PTEN expression by upregulating MicroRNA-21 (miR-21), which is one of the most frequently overexpressed miRNAs in solid tumors.
View Article and Find Full Text PDFPan-Cancer Analysis of PTBP1 to Identify it as a Prognostic and Immunological Biomarker.
Cancer Control
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Department of Orthopedic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi, China.
Objectives: Human cancer is considered to be an important cause of death worldwide. Polypyrimidine tract binding protein 1 (PTBP1) is emerging as a powerful pro-oncogenic factor in bladder and liver cancer; however, no pan-cancer analysis is presently available. Our study aimed to explore PTBP1 expression profiles, prognostic immunological value, and biological functions across various cancers.
View Article and Find Full Text PDFFructose 1,6-bisphosphatase as a promising target of anticancer treatment.
Adv Biol Regul
October 2024
Department of Molecular Physiology and Neurobiology, University of Wrocław, Sienkiewicza 21, 50-335, Wrocław, Poland. Electronic address:
Fructose 1,6-bisphosphatase (FBP) is a regulatory enzyme of gluconeogenesis that also influences in a non-catalytic manner - via protein-protein interactions - cell cycle-dependent events, mitochondria biogenesis and polarization, synaptic plasticity and even cancer progression. FBP reduces glycolytic capacity of cells via blocking HIF-1α transcriptional activity and modulating NF-κB action, and influences oxidative metabolism by binding to c-MYC. Because FBP limits the energy-producing potential of cells and because a reduction of FBP amounts is observed in cancer cells, FBP is considered to be an anti-oncogenic protein.
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