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Secretory clusterin (sCLU) is a type of stress-induced, pro-survival glycoproteinelevated in early-stage cancer. It enhances cancer cell survival and is associatedwith several types of cancer progression. In this study, we measured the PI3K/AKTsignaling activity by determining the phosphorylation level of the AKT protein,namely pAKT. A549 human non-small cell lung carcinoma (NSCLC) cells were treatedwith insulin-like growth factor-1 (IGF-1) for various periods of time. The resultsshowed that IGF-1 activated the PI3K/AKT signaling pathway in the A549 cells ina time-dependent manner. Western blot analysis was performed to determine theexpression of sCLU protein in A549 cells treated with IGF-1. IGF-1 elevated theexpression of sCLU. To determine whether sCLU is required for the IGF-1 activationof the PI3K/AKT signaling pathway, the A549 cells were treated with IGF-1 andsCLU antisense oligonuleotide (sCLU ASO). sCLU ASO blocked the IGF-1 activationof the PI3K/AKT signaling pathway. These results demonstrate that IGF-1 activatesthe P13K/AKT signaling pathway via the upregulation of sCLU. The present studyimplies that this pathway may uncover a new mechanism for cancer progression andreveal new targets for drug development in the treatment of NSCLC.

IGF-1 activates the P13K/AKT signaling pathway via upregulation of secretory clusterin