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VIPR2
VIPR2 Full Name
vasoactive intestinal peptide receptor 2
VIPR2 Introduction
VIPR2 (vasoactive intestinal peptide receptor 2), also known as VPAC2, is a class B G protein-coupled receptor that mediates the biological effects of vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase-activating polypeptide (PACAP). As researchers increasingly focus on neuroimmune communication and tumor microenvironment signaling, VIPR2 has emerged as a clinically relevant target in neuroscience, oncology, and immunology. The receptor is widely expressed in the central nervous system, immune cells, and peripheral tissues, where it regulates intracellular cyclic AMP (cAMP) signaling, cell survival, differentiation, and inflammatory responses. Growing evidence suggests that dysregulated VIPR2 expression or signaling can profoundly alter tissue homeostasis and disease progression, making it an attractive biomarker and therapeutic candidate for precision medicine applications. In recent years, advances in structural biology and AI-assisted protein modeling have further accelerated interest in VIPR2, especially for rational drug design targeting difficult-to-treat cancers and neuropsychiatric disorders.
One of the most important breakthroughs in VIPR2 research comes from studies linking VIPR2 gene microduplication at chromosome 7q36.3 to schizophrenia and neurodevelopmental abnormalities. Overexpression of the VPAC2 receptor has been shown to excessively activate downstream signaling pathways during brain development, potentially disrupting cortical maturation, synaptic plasticity, and sensory information processing. These alterations are particularly relevant to cognitive dysfunction, impaired social behavior, and abnormal neural circuitry formation observed in schizophrenia spectrum disorders and autism-related conditions. Experimental animal and cellular models indicate that hyperactive VIP-VPAC2 signaling may interfere with prefrontal cortex development and neuronal connectivity, especially under conditions of altered PACAP regulation during aging or stress. Because many psychiatric disorders still lack clearly druggable molecular targets, VIPR2 has attracted considerable attention as a promising candidate for mechanistic studies and next-generation neuropsychiatric therapies aimed at restoring balanced neuropeptide signaling.
Beyond the nervous system, VIPR2 has become increasingly important in cancer biology due to its role in tumor growth, migration, metastasis, and immune suppression. In breast cancer models, activation of VIPR2 stimulates PI3Kγ signaling and promotes WAVE2-mediated actin cytoskeleton remodeling, enabling enhanced tumor cell motility and pseudopodia formation. These findings suggest that VIPR2 contributes directly to metastatic progression and may serve as a therapeutic target for limiting cancer dissemination. More recently, pancreatic ductal adenocarcinoma (PDAC) studies demonstrated that VPAC2 signaling promotes both tumor proliferation and an immunosuppressive tumor microenvironment through cAMP/PKA-dependent activation of Piwil2, c-Myc, and TGF-β1 pathways. Importantly, loss of VPAC2 expression sensitized tumors to anti-PD-1 immunotherapy, highlighting the receptor's potential value in combination immunotherapy strategies. With the integration of AlphaFold2-based structural prediction and molecular dynamics simulation, researchers can now better characterize VIPR2-ligand interactions and accelerate the development of highly selective VPAC2 antagonists. These advances position VIPR2 as a high-value therapeutic target with expanding applications in oncology, immunotherapy, and translational drug discovery.
Alternate Names for VIPR2
VIPR2; vasoactive intestinal peptide receptor 2; VPAC2; VPAC2R; VIP-R-2; VPCAP2R; PACAP-R3; DUP7q36.3; PACAP-R-3; C16DUPq36.3
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