Abstract 1792: Upregulation of INSR/IGF1Rby C-myc promotes TSCC tumorigenesis and metastasis through the NF-κB pathway

Abstract

Abstract INSR/IGF1R has been detected to be involved in tumorigenesis and metastasis in various malignancies. The aim of our study was to compare the function role and mechanism of INSR/IGF1R in the progression of tongue squamous cell carcinoma (TSCC). We found that INSR had the same up-regulated expression pattern as IGF1R in TSCC tissues. Up-regulation of INSR/IGF1R was correlated each other and associated with lymph node metastasis and poor prognosis. Functional studies established that INSR/IGF1R knockdown dramatically impeded TSCC in vitro cell growth, migration, invasion and in vivo tumorigenesis and tumor metastasis, whereas ectopic overexpression of INSR/IGF1R enhanced these parameters. INSR/IGF1R promoted TSCC tumorigenesis and metastasis by positively modulating the NF-κB pathway. Furthermore, the up-regulation of INSR and IGF1R in TSCC resulted directly from the binding of C-myc to their promoters. Collectively, our current data demonstrate that the INSR/IGF1R axis, directly targeted by C-myc, plays an important role in the development and progression of TSCC, through NF-κB pathway, and that INSR and IGF1R are potential prognostic factors for TSCC. Citation Format: Anxun Wang, Jingjing Sun, Mei Yu, Zhiyuan Lu, Wei Wang. Upregulation of INSR/IGF1Rby C-myc promotes TSCC tumorigenesis and metastasis through the NF-κB pathway [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1792.