Nuclear IGF1R interacts with NuMA and regulates 53BP1‑dependent DNA double‑strand break repair in colorectal cancer.

ABSTRACT: Nuclear insulin‑like growth factor 1 receptor (nIGF1R) has been associated with poor overall survival and chemotherapy resistance in various types of cancer; however, the underlying mechanism remains unclear. In the present study, immunoprecipitation‑coupled mass spectrometry was performed in an IGF1R‑overexpressing SW480‑OE colorectal cancer cell line to identify the nIGF1R interactome. Network analysis revealed 197 proteins of interest which were involved in several biological pathways, including RNA processing, DNA double‑strand break (DSB) repair and SUMOylation pathways. Nuclear mitotic apparatus protein (NuMA) was identified as one of nIGF1R's colocalizing partners. Proximity ligation assay (PLA) revealed different levels of p53‑binding protein 1 (53BP1)‑NuMA colocalization between I

SUBMITTER: Yang C 

PROVIDER: S-EPMC8250583 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature