AFB1 downregulates IRS1 but paradoxically upregulates IRS2 through positive regulation of the stability of IRS2 and the proteasomal degradation of IRS1 in lung cancer cell lines A549 and SPCA-1.

Reduced insulin receptor substrate-1 (IRS-1) staining in lung adenocarcinoma tissue microarray displayed a significant survival disadvantage, especially within the Kirsten rat sarcoma viral oncogene homolog (KRAS) mutant subgroup.

Results show that ectopic expression of SH2B1 in lung adenocarcinoma (LADC) cell line H1299 cells increased IRS1 expression level. Reduced expression of IRS1 considerably inhibited H1299 cell proliferation, migration, and invasion. These findings suggest that IRS1 plays a role in LADC carcinogenesis.

a specific interaction between PSPH and IRS1 and the dephosphorylation of phospho-IRS-1 by PSPH in lung cancer cells, was identified.

ZNF322A-mediated protein phosphorylation induces autophagosome formation through modulation of IRS1-AKT glucose uptake and HSP-elicited UPR in lung cancer.

Suppression of IRS-1 promotes mammary tumor metastasis to the lung.

lung-specific dual ablation of insulin receptor substrates 1/2 (succumb to tumor burdenIrs1/Irs2) strongly suppresses tumor initiation and dramatically extends the survival of a mouse model of lung cancer with Kras activation and p53 loss. Mice with Irs1/Irs2 loss eventually.