MIIP, also known as migration and invasion inhibitory protein, functions as a tumor-suppressor gene. It plays crucial roles in regulating cell migration, invasion, mitosis, and angiogenesis. MIIP regulates microtubule dynamics by binding to and inhibiting HDAC6, and is also involved in the mitosis checkpoint. It participates in multiple signaling pathways relevant to cancer development, such as the AKT-mTOR pathway, and is located in chromosomal region 1p36, a commonly deleted region in many human cancers [1].

In various cancer types, loss-of-function experiments have revealed MIIP's significance. In hepatocellular carcinoma, low MIIP expression is associated with distant metastasis and poor prognosis, and MIIP can inhibit the malignant progression of the disease by modulating AKT expression [3]. In triple-negative breast cancer, MIIP inhibits angiogenesis, proliferation, and metastasis by directly interacting with ITGB3 and suppressing its downstream signaling [2]. In prostate cancer, MIIP knockdown promotes tumor growth and bone osteolytic lesions, while overexpression inhibits growth via interaction with PP1α and negative modulation of AKT-mTOR signaling [4,5]. In clear cell renal cell carcinoma, MIIP overexpression inhibits proliferation and angiogenesis by negatively regulating the HIF-2α-CYR61 axis [6].

In conclusion, MIIP is a key tumor-suppressor gene. Through model-based research, especially loss-of-function experiments in cancer cell lines and animal models, it has been shown to play important roles in inhibiting the malignant progression of various cancers, including hepatocellular carcinoma, triple-negative breast cancer, prostate cancer, and clear cell renal cell carcinoma. These findings provide potential molecular targets for cancer treatment and highlight the importance of MIIP in cancer research.