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. 2022 Jul 4;18(11):4341–4356. doi: 10.7150/ijbs.71134

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This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

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A schematic overview depicting the potential role of VIP/VIPR1 signaling in controlling HCC development. In normal physiological conditions, VIP/VIPR1 signaling plays a key role in maintaining arginine metabolic homeostasis and growth of the hepatocyte. The ligand VIP binds its Type-1 receptor, VIPR1, then mediates transmembrane signaling transduction. VIP/VIPR1 signaling modulates UC by regulating ASS1 level; additionally, ASS1 may partially participate in regulating pyrimidine synthesis by limiting phosphorylation of CAD, which contributes to normal cell growth and metabolic homeostasis. In contrast, during HCC, VIP/VIPR1 signaling is significantly downregulated due to the decrease/loss of VIPR1, which may be involved in ASS1 reduction. Moreover, ASS1 downregulation caused by inactivation of VIP/VIPR1 signaling can in turn promote HCC proliferation/recurrence through phosphorylation of CAD in an mTOR/p70S6K pathway-dependent manner. Abbreviations: UC: Urea cycle; CAD: Carbamoyl-Phosphate Synthetase 2; ASS1: argininosuccinate synthase.