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Radon and its progeny have been classified as human class I carcinogens by the IARC. However, the mechanisms by which radon induces lung and other cancers, especially the radon-induced Warburg effect, have not been fully elucidated. The aim of this study was to investigate the role of the succinate dehydrogenase subunit A (SDHA)-mediated Warburg effect in (human bronchial epithelial) BEAS-2B cells with malignant transformations induced by long-term radon exposure. Soft agar colony formation and MMP-9 were increased following radon-induced malignant transformation. Additionally, we observed the Warburg effect in BEAS-2B cells following long-term radon exposure, evidenced by increases in the levels of glucose uptake, lactate, and lactate dehydrogenase (LDH). Following radon exposure, the expression of SDHA was decreased, while the levels of HIF-1α and hexokinase-2 (HK2) were increased. Our findings suggested that the SDHA-associated pathway may be involved in mediating the Warburg effect in radon-induced malignant transformation of BEAS-2B.
This article was published in the following journal.
Name: Environmental toxicology
Bromopyruvate (3-BrPA) is a glycolysis inhibitor that has been reported to have a strong anti-tumour effect in many human tumours. Several studies have reported that 3-BrPA could inhibit glioma progre...
The Warburg Effect has emerged as a potential drug target because, in some cancer cell lines, it is sufficient to subvert it in order to kill cancer cells. It has also been shown that the Warburg Effe...
Atrial fibrillation (AF) is the most common sustained arrhythmia. Atrial remodeling, including electrical/structural/autonomic remodeling, plays a vital role in AF pathogenesis. All of these have been...
Increasing evidence confirmed that the Warburg effect plays an important role involved in the progression of malignant tumors. Resibufogenin (RES) has been proved to have a therapeutic effect in multi...
Most tumor cells use aerobic glycolysis (the Warburg effect) to support anabolic growth and promote tumorigenicity and drug resistance. Intriguingly, the molecular mechanisms underlying this phenomeno...
Study purpose is to evaluate treatment outcome and survival in patient with aggressive lymphomas transformed from Follicular Lymphoma.
The primary objective of this study is to to verify the feasibility of obtaining and comparing two epithelia in two populations based on the following experiments: - Differentiation of...
This study is meant to compare two routine diagnostic approaches in patients with bronchial asthma. Patients are challenged with methacholine in order to measure their bronchial response. ...
The purpose of this research study is to evaluate the safety, effect, and pharmacology of C1 Esterase Inhibitor (human) in kidney transplant patients with Antibody-Mediated Rejection (AMR)...
This is a randomised, controlled, cross-over study to determine the effect of indirect bronchial challenge testing upon volatile organic compounds (VOCs) in the exhaled breath of adults wi...
The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.
Thermal destruction of the excess bronchial SMOOTH MUSCLE tissue with heat delivered through a catheter assembly attached to a BRONCHOSCOPE. It is often used to control BRONCHIAL HYPERREACTIVITY in severe ASTHMA for better AIRWAY MANAGEMENT.
Left bronchial arteries arise from the thoracic aorta, the right from the first aortic intercostal or the upper left bronchial artery; they supply the bronchi and the lower trachea.
Retrovirus-associated DNA sequences (mos) originally isolated from the Moloney murine sarcoma virus (Mo-MSV). The proto-oncogene mos (c-mos) codes for a protein which is a member of the serine kinase family. There is no evidence as yet that human c-mos can become transformed or has a role in human cancer. However, in mice, activation can occur when the retrovirus-like intracisternal A-particle inserts itself near the c-mos sequence. The human c-mos gene is located at 8q22 on the long arm of chromosome 8.
Hormonally active polypeptides that can induce the transformed phenotype when added to normal, non-transformed cells. They have been found in culture fluids from retrovirally transformed cells and in tumor-derived cells as well as in non-neoplastic sources. Their transforming activities are due to the simultaneous action of two otherwise unrelated factors, TRANSFORMING GROWTH FACTOR ALPHA and TRANSFORMING GROWTH FACTOR BETA.
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