Irs1, or Insulin Receptor Substrate 1, is a crucial signal transduction adapter. It facilitates extracellular signal transduction from insulin-like growth factor-1 receptor and its family members to downstream proteins. IRS1 is involved in the insulin signaling pathway, which is essential for the hormonal control of metabolism [5]. Mutations in this gene have been associated with an increased ability to develop type 2 diabetes, highlighting its importance in metabolic health [4].

In cancer research, IRS1 has been found to play diverse roles. In thyroid cancer, it is highly expressed, promoting metastasis through epithelial-mesenchymal transition (EMT) and the PI3K/AKT pathway, suggesting it could be a stratified marker and therapeutic target [1]. In oral squamous cell carcinoma (OSCC), IRS1 is also highly expressed, and its silencing decreases cell proliferation, increases apoptosis, and hinders EMT through the p53/Line-1 signaling pathway [2]. In ovarian cancer, repressing IRS1/2 by NT157 inhibits malignant behaviors by inactivating the PI3K/AKT/mTOR pathway and inducing autophagy [3]. In esophageal squamous cell carcinoma, IRS1 expression is associated with lymph node metastases and prognosis, with overexpression negatively associated with metastasis [6].

In conclusion, Irs1 is essential for insulin-mediated signal transduction and metabolism. Its role in various cancers, as revealed through functional studies, shows its potential as a biomarker and therapeutic target in oncology. The study of Irs1 knockout or conditional knockout mouse models could further clarify its functions in normal and disease-related biological processes.