We analyzed the genetic alterations of VHL, HGF/SF, and Met genes and the expression pattern of HGF/SF and Met protein in 26 renal cell carcinomas (RCCs). We found five mutations of the VHL gene and frequent LOH (50%) only in non-papillary clear cell RCC. We found six cases in which the CpG island of VHL was methylated. In addition, one missense mutation of the HGF/SF gene was detected in clear cell RCC. HGF/SF and Met protein were expressed in 84.6% and 80.7% of RCCs, respectively. All of the cases with the genetic alterations of VHL or HGF/SF demonstrated strong expression of HGF/SF and Met protein in RCC cells. Statistically, genetic alterations of VHL and HGF/SF were significantly correlated with HGF/SF and Met expression (Fisher's exact test, p=0.022 and p=0.0070). Thus, these results strongly suggest that the expression of HGF/SF and Met protein is closely associated with the genetic alterations of VHL and HGF/SF in primary RCCs.
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http://dx.doi.org/10.1034/j.1600-0463.2002.100305.x | DOI Listing |
Front Immunol
November 2024
Department of Otolaryngology, Head and Neck Surgery, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Background: Studies indicated that diverse cellular mechanisms including epithelial migration and hyper-proliferation, inflammatory responses, and enzymatic bone erosion were involved in the pathogenesis of cholesteatoma. S100A8 and S100A9, which are Ca2+-binding proteins belonging to the S100 family, can trigger the signaling pathways involved in the inflammatory processes, and a variety of cellular processes includes cell cycle progression, proliferation, and cell migration. However, the role of S100A8 and S100A9 and their associated inflammation and other signaling pathways in cholesteatoma have not been investigated yet.
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January 2024
Rosalind and Morris Goodman Cancer Institute, McGill University, Montreal, QC H3A 1A3, Canada.
Brain tumors represent a heterogeneous group of neoplasms characterized by a high degree of aggressiveness and a poor prognosis. Despite recent therapeutic advances, the treatment of brain tumors, including glioblastoma (GBM), an aggressive primary brain tumor associated with poor prognosis and resistance to therapy, remains a significant challenge. Receptor tyrosine kinases (RTKs) are critical during development and in adulthood.
View Article and Find Full Text PDFEur J Cancer
November 2022
Department of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Peking University, Beijing, 100191, China. Electronic address:
Introduction: Glioma is the most common and most invasive primary central nervous system tumour, and it is urgent to develop new specific therapeutic targets. Studies have confirmed that epithelial-derived tumour cells promote tumour cell proliferation and metastasis by secreting a large number of immunoglobulins (Igs), but the role of tumour-derived Igs in glioma has never been reported.
Methods: The Gene Expression Profiling Interactive Analysis and Chinese Glioma Genome Atlas databases were used to analyse the Ig transcription and its correlation with the prognosis of patients with glioma.
Life Sci Alliance
July 2022
University of Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019, UMR 9017, CIIL, Center for Infection and Immunity of Lille, Lille, France
Hepatocyte growth factor/scatter factor (HGF/SF) and its cognate receptor MET play several essential roles in embryogenesis and regeneration in postnatal life of epithelial organs such as the liver, kidney, lung, and pancreas, prompting a strong interest in harnessing HGF/SF-MET signalling for regeneration of epithelial organs after acute or chronic damage. The limited stability and tissue diffusion of native HGF/SF, however, which reflect the tightly controlled, local mechanism of action of the morphogen, have led to a major search of HGF/SF mimics for therapy. In this work, we describe the rational design, production, and characterization of K1K1, a novel minimal MET agonist consisting of two copies of the kringle 1 domain of HGF/SF in tandem orientation.
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May 2022
Department of Cell Biology, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
SMER28 (Small molecule enhancer of Rapamycin 28) is an autophagy-inducing compound functioning by a hitherto unknown mechanism. Here, we confirm its autophagy-inducing effect by assessing classical autophagy-related parameters. Interestingly, we also discovered several additional effects of SMER28, including growth retardation and reduced G1 to S phase progression.
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