SOCS-1, a negative regulator of the JAK/STAT pathway, is silenced by methylation in human hepatocellular carcinoma and shows growth-suppression activity

By Hirohide Yoshikawa, K. Matsubara, G. Qian, P. Jackson, J. Groopman, J. Manning, C. Harris, J. Herman. Nature Genetics, 2001

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MicroRNA-155 functions as an OncomiR in breast cancer by targeting the suppressor of cytokine signaling 1 gene. (2010, background): “socs1 has been reported to be a tumor suppressor that negatively regulates cell growth and transformation of several cancer cells (30, 31).”
Stat proteins and oncogenesis. (2002, background): “recently showed that methylation-induced silencing of the SOCS1 gene leads to constitutive STAT3 activation in a hepatocellular carcinoma–derived cell line (36).”
RNA N6‐methyladenosine methyltransferase‐like 3 promotes liver cancer progression through YTHDF2‐dependent posttranscriptional silencing of SOCS2 (2018, background): “SOCS2 is a member of the suppressor of cytokine signaling family, which serves as a cytokine-inducible negative regulator of the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway.((36)) We found that knockdown of METTL3 increased SOCS2 protein expression and consequent”
The role of IL-6 and STAT3 in inflammation and cancer. (2005, background): “As mentioned earlier, in some tumour cells these negative effectors (specifically SOCS1) are inactivated by epigenetic silencing of their promoters [73,80].”