The suppressor of cytokine signaling 6 (SOCS6) expression level might be an important indicator for predicting survival in patients with gastrointestinal stromal tumor (GIST), as published in Diagnostic Pathology.
Researchers from China found an association between the expression level of SOCS6 and tumor size (P =.001). No association was found between the expression level of SOCS6 and other clinicopathological parameters, such as age, gender, tumor location, necrosis of tumor, mitotic index, and National Institutes of Health tumor risk grade.
They also observed a correlation between low expression levels of SOCS6 and worse overall survival (OS) rates in patients with GIST. Patients with GIST and high SOCS6 expression levels (n=102) had a 1-year, 3-year, and 5-year OS of 97.79%, 95.75%, and 89.62%, respectively, and mean survival rates of 135.00 ± 5.30 months.
These rates decreased to 96.04%, 89.49%, and 78.95%, respectively, in patients with GIST with low SOCS6 expression levels (n=153). In this group, the mean survival rates were 95.56 ± 4.56 months.
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The study also reported a correlation between low expression levels of SOCS6 and worse recurrence-free survival (RFS) rates in patients with GIST. Patients with GIST and high SOCS6 expression levels had a 1-year, 3-year, and 5-year RFS of 96.96%, 94.81%, and 84.79%, respectively, and mean RFS rates of 129.49 ± 5.73 months.
These rates decreased to 93.36%, 85.62%, and 73.30%, respectively, in patients with GIST and low SOCS6 expression levels. In this group, the mean survival was 91.27 ± 4.64 months. Further analysis suggested that low expression of SOCS6 was an independent predictive factor for OS and RFS in patients with GIST.
“As one of the ubiquitous E3 ubiquitin ligases, SOCS6 could promote the ubiquitin-mediated degradation of proteins by binding with phosphorylated tyrosine receptors or signaling proteins,” the authors explained.
In addition, mechanistic studies have been supporting ubiquitin-independent roles for SOCS6 that lead to the negative regulation of signaling pathways, including those mediated by the extracellular signal-regulated kinase 1/2 and the mitogen-activated protein kinase p38.
As the next step, Ouyang et al aim to investigate the role of SOCS6 in the proliferation of GIST cells and the molecular mechanisms underlying such effect, if any. They also aim to study the potential involvement of SOCS6 in the acquisition of resistance to drugs, such as imatinib.
Ouyang J, An T, Wang Y, et al. Down-regulation of SOCS6: an unfavorable prognostic factor for gastrointestinal stromal tumor proven by survival analysis. Diagn Pathol. 2021;16(1):113. doi:10.1186/s13000-021-01172-6