SH2B1, an adaptor protein associated with obesity, is closely related to the occurrence and development of a variety of tumors. To investigate the clinical significance of SH2B1 in colorectal cancer (CRC), expression of SH2B1 in colorectal normal tissues, adenomas, paracarcinoma tissues, carcinoma tissues, and metastatic tissues from 1003 CRC patients was detected by immunohistochemistry (IHC). The prediction power of SH2B1 for CRC prognosis was evaluated by Kaplan-Meier survival analysis and Cox regression model. Results revealed the expression of SH2B1 in carcinoma tissues was significantly higher than that in other tissues. High expression of SH2B1 was an independent risk factor for both disease-free survival (DFS) and disease-specific survival (DSS) and predicted unfavorable prognosis of CRC as well as poor chemotherapeutic response. Conclusively, SH2B1 can serve as an effective predictor for CRC survival and chemotherapeutic outcomes.
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http://dx.doi.org/10.4149/neo_2021_201015N1092 | DOI Listing |
Endocrinology
January 2025
Graduate Program in Cellular and Molecular Biology.
SH2B1β is a multifunctional scaffold protein that modulates cytoskeletal processes such as cellular motility and neurite outgrowth. To identify novel SH2B1β-interacting proteins involved in these processes, a yeast two-hybrid assay was performed. The C-terminal 159 residues of the cytoskeleton structural protein, βIIΣ1-spectrin, interacted with the N-terminal 260 residues of SH2B1β, a region implicated in SH2B1β enhancement of cell motility and localization at the plasma membrane.
View Article and Find Full Text PDFAdv Sci (Weinh)
August 2024
Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
SH2B1 mutations are associated with obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease (MASLD) in humans. Global deletion of Sh2b1 results in severe obesity, type 2 diabetes, and MASLD in mice. Neuron-specific restoration of SH2B1 rescues the obesity phenotype of Sh2b1-null mice, indicating that the brain is a main SH2B1 target.
View Article and Find Full Text PDFCell Rep Med
August 2023
University of Cambridge Metabolic Research Laboratories, Wellcome-MRC Institute of Metabolic Science and NIHR Cambridge Biomedical Research Centre, Addenbrooke's Hospital, Cambridge CB2 0QQ, UK. Electronic address:
Clin Exp Pharmacol Physiol
October 2023
Department of Cardiology, Hubei Key Laboratory of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan University, Wuhan, China.
This study mainly explored the effect and mechanism of Src homology 2 (SH2) B adaptor protein 1 (SH2B1) on cardiac glucose metabolism during pressure overload-induced cardiac hypertrophy and dysfunction. A pressure-overloaded cardiac hypertrophy model was constructed, and SH2B1-siRNA was injected through the tail vein. Haematoxylin and eosin (H&E) staining was used to detect myocardial morphology.
View Article and Find Full Text PDFBrain
October 2023
Faculdade de Ciências e Tecnologia, Universidade dos Açores, 9500-321 Ponta Delgada, Portugal.
Transcriptional dysregulation has been described in spinocerebellar ataxia type 3/Machado-Joseph disease (SCA3/MJD), an autosomal dominant ataxia caused by a polyglutamine expansion in the ataxin-3 protein. As ataxin-3 is ubiquitously expressed, transcriptional alterations in blood may reflect early changes that start before clinical onset and might serve as peripheral biomarkers in clinical and research settings. Our goal was to describe enriched pathways and report dysregulated genes, which can track disease onset, severity or progression in carriers of the ATXN3 mutation (pre-ataxic subjects and patients).
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