CHFR acts as a tumor suppressor gene, which is frequently inactivated caused by its promoter hypermethylation in various solid tumors. Although a recent study showed that CHFR hypermethylation was a frequent event in acute myeloid leukemia (AML) and correlated with adverse clinical outcome, herein, we found that CHFR methylation was a rare event in patients with myeloid malignancies (including AML, chronic myeloid leukemia, and myelodysplastic syndromes), but its expression may serve as an independent prognostic biomarker in AML. CHFR expression was assessed by real-time quantitative PCR, whereas CHFR methylation was detected by methylation-specific PCR and bisulfite sequencing PCR. In AML patients, lower CHFR expression was associated with lower complete remission (CR) rate, and CHFR expression was significantly increased in CR after chemotherapy. Moreover, patients with lower CHFR expression showed shorter overall survival and leukemia-free survival, and multivariate analysis confirmed that lower CHFR expression was an independent risk factor in AML. Importantly, the prognostic value of CHFR expression was validated using the published Gene Expression Omnibus datasets. Notably, CHFR promoter was nearly unmethylated in patients with myeloid malignancies. Our findings revealed that lower CHFR expression was independently associated with unfavorable prognosis in AML. Moreover, aberrant CHFR promoter methylation was a rare event in myeloid malignances.
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http://dx.doi.org/10.1002/jcp.26253 | DOI Listing |
Nat Commun
October 2023
Department of Pharmacology and Regenerative Medicine and The Center of Lung and Vascular Biology, University of Illinois College of Medicine, Chicago, IL, USA.
Vascular endothelial cadherin (VE-cadherin) expressed at endothelial adherens junctions (AJs) is vital for vascular integrity and endothelial homeostasis. Here we identify the requirement of the ubiquitin E3-ligase CHFR as a key mechanism of ubiquitylation-dependent degradation of VE-cadherin. CHFR was essential for disrupting the endothelium through control of the VE-cadherin protein expression at AJs.
View Article and Find Full Text PDFJ Inflamm Res
July 2023
Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan, People's Republic of China.
Background: Coronary artery disease (CAD) is a multifactorial immune disease, but research into the specific immune mechanism is still needed. The present study aimed to identify novel immune-related markers of CAD.
Methods: Three CAD-related datasets (GSE12288, GSE98583, GSE113079) were downloaded from the Gene Expression Integrated Database.
BMC Gastroenterol
April 2023
Department of Gastroenterology, The Fifth Affiliated Hospital of Wenzhou Medical University and Lishui Municipal Central Hospital, Lishui, 323000, Zhejiang Province, China.
Tumor suppressor gene CHFR (The Checkpoint with Forkhead-associated and Ring finger domains) is a mitotic checkpoint and frequently hypermethylated in gastric cancer. Our previous study found CHFR played a certain extent pro-tumor function in gastric cancer. However, little is known about the underlying mechanism.
View Article and Find Full Text PDFExp Mol Pathol
April 2022
University Hospital of Saint Etienne, North Hospital, Department of Pathology, Avenue Albert Raimond, 42055 Saint Etienne, Cedex 2, France; University Hospital of Saint Etienne, North Hospital, Molecular Biology of Tumors Unit, Avenue Albert Raimond, 42055 Saint Etienne, Cedex 2, France.
Lung adenocarcinoma grading has gained interest in the past years. Recently a three-tier tumor grading was proposed showing that it is related to patients' prognosis. Nevertheless, the underlying molecular basis of this morphological grading remains partly unknown.
View Article and Find Full Text PDFCancers (Basel)
November 2021
Department of Molecular Pharmacology & Experimental Therapeutics, Mayo Clinic, Rochester, MN 55905, USA.
The poly(ADP-ribose) binding protein CHFR regulates cellular responses to mitotic stress. The deubiquitinase UBC13, which regulates CHFR levels, has been associated with better overall survival in paclitaxel-treated ovarian cancer. Despite the extensive use of taxanes in the treatment of ovarian cancer, little is known about expression of CHFR itself in this disease.
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