The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia

Abstract

Cytokines are pleiotropic signaling molecules that execute an essential role in cell-to-cell communication through binding to cell surface receptors. Receptor binding activates intracellular signaling cascades in the target cell that bring about a wide range of cellular responses, including induction of cell proliferation, migration, differentiation, and apoptosis. The Janus kinase and transducers and activators of transcription (JAK/STAT) signaling pathways are activated upon cytokines and growth factors binding with their corresponding receptors. The SOCS family of proteins has emerged as a key regulator of cytokine signaling, and SOCS insufficiency leads to constitutive activation of JAK/STAT signaling and oncogenic transformation. Dysregulation of SOCS expression is linked to various solid tumors with invasive properties. However, the roles of SOCS in hematological malignancies, such as leukemia, are less clear. In this review, we discuss the recent advances pertaining to SOCS dysregulation in leukemia development and progression. We also highlight the roles of specific SOCS in immune cells within the tumor microenvironment and their possible involvement in anti-tumor immunity. Finally, we discuss the epigenetic, genetic, and post-transcriptional modifications of SOCS genes during tumorigenesis, with an emphasis on leukemia.

Antineoplastic activity of biogenic silver and gold nanoparticles to combat leukemia: Beginning a new era in cancer theragnostic

“…As such, it is easy to distinguish between acute lymphocytic leukemia (ALL); and acute myeloid leukemia (AML); both types have chances to become chronical and categorized as chronic lymphocytic leukemia (CLL); and chronic myeloid leukemia (CML). Moreover, each of these types has different subcategorizes [ 14 , 15 ].…”

Regulation of mi-RNAs Target Cancer Genes Between Exercise and Non-exercise in Rat Rheumatoid Arthritis Induction: Pilot Study

“… 35 In chronic rheumatoid arthritis inflammation, SOCSs can alter the expression and regulate JAK/STAT as mutation induces leukemia. 38 By contrast, with exercise JAK/STAT phosphorylation may increase, while satellite cell proliferation differentiated with transcription of the activating cell cycle. 39 Thus, the EX + PIA group could have less SOCS 6 expression than the N-EX + PIA group.…”

Multiomics to investigate the mechanisms contributing to repression of PTPRC and SOCS2 in pediatric T‐ALL: Focus on miR‐363‐3p and promoter methylation

“…Thus far, there are only few reports about the regulatory role of miRNAs in the repression of SOCS genes in leukemia and there is no evidence of such regulation in T-ALL. 37 The only miRNA described as a negative regulator of SOCS2 expression in leukemia, is miR-486, reported to be upregulated in acute myeloid leukemia cell lines. 38 Here, we present for the first time that the expression of a gene from the SOCS family is regulated by aberrantly expressed miRNAs in T-ALL and we show that SOCS2 is a direct target of miR-363-3p.…”