Breast cancer, a global health issue, is marked by increasing prevalence and diverse molecular subtypes, which complicate effective treatment strategies. A relevant aspect in breast cancer etiology and development is epidermal growth factor receptor (EGFR) dysregulation. This review examines the intricate regulation of EGFR, focusing on the roles of signaling molecules and microRNAs (miRNAs) in EGFR regulation in breast cancer. The paper delves into the molecular mechanisms underlying EGFR dimerization, activation, and downstream routes for signaling, emphasizing the roles of signaling molecules such as Cbl and Cdc42. Furthermore, the emerging role of miRNAs as essential modulators of gene activity in breast cancer is discussed, focusing on differential expression patterns and functional implications in tumor progression. By elucidating the regulatory networks involving EGFR, signaling molecules, and miRNAs, the current review offers insights into potential therapeutic targets and avenues for future research in breast cancer. • EGFR dysregulation is a key driver of breast cancer pathogenesis. • c-Cbl promotes EGFR degradation through ubiquitination. • Cdc42 impairs c-Cbl, sustaining EGFR signaling. • MicroRNAs modulate breast cancer progression as oncogenes or tumor suppressors. • Targeting EGFR–c-Cbl–Cdc42–miRNA networks presents new therapeutic avenues.
Andam et al. (Sat,) studied this question.