Lipg-KO Mouse

Lipg, also known as endothelial lipase (EL), is a crucial gene in the human body. It functions predominantly as a phospholipase with low levels of triglyceride lipase activity. Lipg plays an essential role in lipoprotein metabolism and is involved in metabolic syndromes such as the inflammatory response and atherosclerosis [1].

In breast cancer, studies have shown that the risk of breast cancer increases with increasing levels of LIPG, especially in pre-menopausal, Luminal A, HER2-negative, non-postpartum breast cancers, and in women with high total cholesterol levels [2]. LIPG-promoted lipid storage can mediate adaptation to oxidative stress in breast cancer cells, and high LIPG expression is associated with shorter metastasis-free survival in node-negative, untreated breast cancer patients [3].

In lung adenocarcinoma, LIPG expression is higher in tumor tissues, especially in certain patient subgroups, and high expression predicts a poor prognosis. It may affect the development of lung adenocarcinoma through lipid metabolism and immune system regulation, and is correlated with immune infiltrates and response to antitumor drugs [4].

In colorectal cancer, ZDHHC1 can downregulate LIPG and inhibit cancer cell growth [5].

In human basal-like triple-negative breast cancer, LIPG is overexpressed and is required for tumorigenicity and metastasis, and its phospholipase activity can be targeted to suppress tumor formation [6,7]. Additionally, in some ethnic groups, LIPG SNPs and their haplotypes are associated with serum lipid levels [8].

In conclusion, Lipg is involved in multiple biological processes, especially lipoprotein metabolism and related metabolic syndromes. Its role in various cancers, such as breast, lung, and colorectal cancers, has been increasingly recognized through research. The study of Lipg using different models helps to understand its function in disease development, providing potential targets for cancer treatment and management of metabolic diseases.