ArticleClinical and translational medicine2024
JCAD deficiency delayed liver regenerative repair through the Hippo-YAP signalling pathway.
Article in Clinical and translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Study of JCAD for prognosis and immune infiltration in hepatocellular carcinoma.Frontiers in immunology · 2026Article
- Influencing factors and mechanism of hepatocyte regeneration.Journal of translational medicine · 2025Review
- Quercetin alleviates rifampicin-induced hepatocyte injury by modulating the Hippo-YAP signaling pathway.Frontiers in medicine · 2025Article
- Correspondence on Letter regarding "Both liver parenchymal and non-parenchymal cells express JCAD proteins under various circumstances".Clinical and molecular hepatology · 2024Article
- JCAD deficiency delayed liver regenerative repair through the Hippo-YAP signalling pathway.Clinical and translational medicine · 2024Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND AND
aimsLiver regeneration retardation post partial hepatectomy (PH) is a common clinical problem after liver transplantation. Identification of key regulators in liver regeneration post PH may be beneficial for clinically improving the prognosis of patients after liver transplantation. This study aimed to clarify the function of junctional protein-associated with coronary artery disease (JCAD) in liver regeneration post PH and to reveal the underlying mechanisms.
methodsJCAD knockout (JCAD-KO), liver-specific JCAD-KO (Jcad
resultsBoth global and liver-specific JCAD deficiency postponed liver regeneration after PH as indicated by reduced gene expression of cell cycle transition and DNA replication. Prolonged retention in G1 phase and failure to transition over the cell cycle checkpoint in JCAD-KO cell line was indicated by a FUCCI live-imaging system as well as pharmacologic blockage. JCAD replenishment by adenovirus reversed the impaired DNA synthesis in JCAD-KO primary hepatocyte in exposure to EGF, which was abrogated by a Yes-associated protein (YAP) inhibitor, verteporfin. Mechanistically, JCAD competed with large tumour suppressor 2 (LATS2) for WWC1 interaction, leading to LATS2 inhibition and thereafter YAP activation, and enhanced expression of cell cycle-associated genes.
conclusionJCAD deficiency led to delayed regeneration after PH as a result of blockage in cell cycle progression through the Hippo-YAP signalling pathway. These findings uncovered novel functions of JCAD and suggested a potential strategy for improving graft growth and function post liver transplantation. KEY POINTS: JCAD deficiency leads to an impaired liver growth after PH due to cell division blockage. JCAD competes with LATS2 for WWC1 interaction, resulting in LATS2 inhibition, YAP activation and enhanced expression of cell cycle-associated genes. Delineation of JCADHippoYAP signalling pathway would facilitate to improve prognosis of acute liver failure and graft growth in living-donor liver transplantation.
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