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.

Download full-text PDF

Source
http://dx.doi.org/10.4149/neo_2021_201015N1092DOI Listing

Publication Analysis

Top Keywords

expression sh2b1
12
high expression
8
adaptor protein
8
sh2b1
8
colorectal cancer
8
sh2b1 colorectal
8
carcinoma tissues
8
tissues
6
crc
5
expression sh2b
4

Similar Publications

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 PDF

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 PDF

Chromosomal deletions on 16p11.2 encompassing SH2B1 are associated with accelerated metabolic disease.

Cell 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:

Article Synopsis
  • New treatments are needed for obesity and type 2 diabetes (T2D) linked to specific genetic mechanisms, particularly a deletion on chromosome 16p11.2 that affects the SH2B1 gene involved in hormone signaling.
  • Studies from large biobanks in the UK and Estonia reveal that individuals with this genetic deletion experience higher body mass index (BMI) and greater rates of T2D, with onset occurring earlier and poorer glycemic control compared to matched controls.
  • Additionally, these deletion carriers show increased levels of a kidney function biomarker, indicating a higher risk of kidney issues, suggesting that therapies to boost leptin and insulin signaling could be beneficial for them.
View Article and Find Full Text PDF

Effect of SH2B1 on glucose metabolism during pressure overload-induced cardiac hypertrophy and cardiac dysfunction.

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 PDF

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).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!