Hif1an, also known as hypoxia-inducible factor 1-alpha subunit suppressor, plays a crucial role in regulating hypoxia-inducible factor 1-alpha (HIF-1α) stability and transcriptional action. It is involved in the oxygen-sensing pathway, with the PHD family of oxygen-dependent prolyl hydroxylases (where Hif1an may be related) playing a pivotal role in regulating HIF stability. Hif1an's function is significant in various biological processes such as development, metabolism, inflammation, and integrative physiology, and its inappropriate expression is associated with cancer development and immune control [2].

In breast cancer, lower Hif1an expression was observed in cancer cells compared to normal specimens, and higher Hif1an expression was associated with good overall survival. Also, Hif1an expression was closely related to chemokines and immune cell infiltration including neutrophils, macrophages, etc., and highly correlated with immunological indicators of T-cell exhaustion [1].

In keloid formation, circSLC8A1 regulates the miR-181a-5p/Hif1an axis to restrain the biological functions of human keloid fibroblasts, suggesting Hif1an's role in this fibrotic disease [3].

In choriocarcinoma, METTL3 promotes miR-21-5p maturation in an m6A-dependent manner, which degrades Hif1an, activating the HIF1A/VEGF pathway and accelerating cancer progression [4].

In hypertrophic scar formation, Rynchopeterine inhibits the formation of hypertrophic scars by up-regulating Hif1an expression through inhibiting miR-21 [5].

In conclusion, Hif1an is a key regulator of HIF-1α and is involved in multiple biological processes. Its dysregulation is associated with various diseases, especially cancer and fibrotic disorders. Studies on Hif1an contribute to understanding the molecular mechanisms of these diseases, potentially providing new therapeutic targets.