Vipr1-flox Mouse

Vipr1, also known as the vasoactive intestinal peptide type-I receptor, is a G protein-associated receptor. It is involved in various biological processes. VIP, which binds to Vipr1, is released during immunologic and inflammatory responses, and Vipr1 is present on immune cells like mast cells, macrophages, B cells, and T cells, playing a role in immunomodulation [8]. It also has a part in maintaining gut microbiota homeostasis, as enteric neurons expressing VIP activate fut2 expression via the Erk1/2-c-Fos pathway through Vipr1 on intestinal epithelial cells, regulating α1,2-fucosylation [4].

In cancer research, Vipr1 shows potential tumor-suppressing roles. In lung adenocarcinoma, its overexpression significantly inhibits the growth, migration, and invasion of H1299 cells [1]. In hepatocellular carcinoma (HCC), the expression of Vipr1 is downregulated, and its activation suppresses HCC progression by regulating arginine and pyrimidine metabolism [2]. Also, the lncRNA-AC079061.1/Vipr1 axis may suppress HCC development [3]. Machine-learning-based analysis identified Vipr1 as a diagnostic biomarker for HCC, and its expression is positively correlated with several immune cells [5]. Epigenetic modifications, such as promoter methylation and H3K27 deacetylation, regulate Vipr1 transcription in HCC, and its overexpression causes cell cycle arrest, promotes apoptosis, and inhibits cell proliferation and tumor growth in HCC [6,7].

In conclusion, Vipr1 has diverse essential functions in immunomodulation and maintaining gut microbiota homeostasis. In cancer, especially in lung adenocarcinoma and HCC, Vipr1 appears to act as a tumor suppressor. Research on Vipr1, including through gene-knockout models (although not specifically detailed in the provided references), helps understand its role in disease mechanisms, potentially providing new strategies for cancer diagnosis and treatment.