Hamp-KO Mouse

HAMP, encoding hepcidin antimicrobial peptide, is a key gene in regulating systemic iron homeostasis. Hepcidin, as a peptide hormone, binds to ferroportin, an iron exporter, leading to its internalization and degradation, thus controlling cellular iron efflux. This post-translational regulation of ferroportin by hepcidin forms a homeostatic loop for iron regulation [4,6].

In gastric cancer, HAMP mRNA is more highly expressed in cancer cells and tumor tissues than in normal tissues. High HAMP expression is associated with poor overall survival and is related to immune cell infiltration levels, suggesting it may be an independent prognostic biomarker through the immune pathway [1].

In non-small cell lung cancer, HAMP expression is increased in cancer cells and tissues. Gain-and loss-of-function experiments show that HAMP promotes cell proliferation, invasion, and migration by activating the NF-κB pathway, which is negatively modulated by miR-873-5p [2].

In hepatocellular carcinoma, HAMP has the potential to diagnose the disease, predict PD-(L)1 immunotherapy sensitivity, and is positively correlated with the infiltration of 18 major immune cells and the expression of 2 important immune checkpoints [3].

In type 2 diabetes, differences in DNA methylation of HAMP in blood cells may predict the development of the disease [7]. Mutations in HAMP can cause atypical juvenile hereditary hemochromatosis, which may be misdiagnosed as type 1 diabetes [5].

In conclusion, HAMP plays a crucial role in iron metabolism and is significantly associated with multiple diseases such as gastric cancer, non-small cell lung cancer, hepatocellular carcinoma, type 2 diabetes, and juvenile hereditary hemochromatosis. Research on HAMP provides insights into understanding the mechanisms of these diseases and potential biomarker discovery.