Research Paper Volume 13, Issue 4 pp 5442—5460

Clinical and genomic characteristics of metabolic syndrome in colorectal cancer

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.

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.