ATG12-dependent autophagy is promoted by the erb-b2 receptor tyrosine kinase 2 (ERBB2), contributing to breast cancer cells' resistance to treatment

Abstract

The erb-b2 receptor tyrosine kinase 2 (ERBB2), a member of the epidermal growth factor receptor (EGFR) family, is overexpressed in a variety of malignancies (radio- and chemotherapy)., While the fundamental processes are yet unknown, treatment resistance does. Autophagy is well-known.to increase resistance to cancer therapy. In this research, we show that ERBB2 rises. Several autophagy genes, such as ATG12 (autophagy-related 12), are expressed, which encouragesautophagy reliant on ATG12. We make it clear that lapatinib, a dual EGFR and ERBB2 inhibitor autophagy was encouraged in cells that only expressed EGFR, but was inhibited in cells that only expressed ERBB2. Furthermore, 35 genes in the canonical autophagy pathway were analyzed from the breast cancer database. Demonstrates that a low relapse-free survival is connected with the overexpression of ATG12 and MAP1LC3B.Likelihood of patients having.