Research Paper Volume 13, Issue 4 pp 5442—5460

Clinical and genomic characteristics of metabolic syndrome in colorectal cancer

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Figure 5. IL6 promotes oncogenic growth in CRC by stimulating mTOR signaling. (A). GSEA of IL6 in the TCGA CRC cohort; (B). Immunohistochemical staining of IL6 in MetS and non-MetS CRC patients; IL6 promotes growth-factor-induced migration (C) and invasion of CRC cells (D). Cancer cells with or without IL6 overexpression were treated with or without PP242; (E) IL6 promoted mTOR signaling in colorectal cancer cells. SW480 and DLD1 expressing ectopic IL6 or vector were analyzed for mTOR signaling by immunoblotting for P-mTOR and P-S6K. GAPDH was used as a loading control; (F) Pharmacological inhibition of mTOR signaling by PP242 abrogated IL6 overexpression-induced activation of mTOR signaling. SW480 and DLD1 cells were transfected with IL6 shRNAs or a control shRNA and then treated with PP242. Their effect on mTOR signaling was analyzed by immunoblotting.