Irs1, short for Insulin receptor substrate 1, is a crucial signal transduction adapter. It is essential for extracellular signal transduction from insulin-like growth factor-1 receptor and its family members to downstream proteins, playing a vital role in the regulation of metabolism by insulin [4]. The protein is involved in multiple pathways such as the phosphoinositide 3-kinase (PI3K)/AKT pathway, which is important for cell growth, survival, and metabolism [1,3].

Irs1 has been found to be highly expressed in several cancers. In thyroid cancer, its high expression is associated with distant metastasis and advanced clinical stages, promoting cancer cell migration, invasion, and colony formation through epithelial-mesenchymal transition (EMT) and the PI3K/AKT pathway [1]. In oral squamous cell carcinoma (OSCC), Irs1 is also highly expressed, and its silencing can decrease cell proliferation, increase apoptosis, and hinder EMT through the p53/Line-1 signaling pathway [2]. In ovarian cancer, inhibiting Irs1/2 with NT157 can suppress malignant behaviors by inactivating the PI3K/AKT/mTOR pathway and inducing autophagy [3]. In esophageal squamous cell carcinoma, Irs1 expression is related to lymph node metastases and prognosis, with decreased expression predicting poor overall survival [5].

In conclusion, Irs1 is a key molecule in insulin-related signal transduction and metabolism regulation. Studies, especially those on cancer, show its significant role in tumorigenesis and metastasis, suggesting that it could be a potential therapeutic target for various cancers [1,2,3,5].