Progress in Research on CNPY2 in Diseases

Chen, Ke-Qian; Zhang, Yuqing; Wang, Zongbao; Wang, Shuzhi

doi:10.2174/1389557523666230601094149

Cited by 2 publications

(3 citation statements)

References 74 publications

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“…Canopy homolog 2 (CNPY2) is an interesting protein and angiogenic growth factor which is present in ER lumen, participating in ER stress, and is likely to play a role in NASH-associated liver cancer progression [ 47 , 48 ]. This molecular target shows promise in addressing hepatocarcinogenesis and serves as a valuable prognostic indicator for various neoplasms [ 49 ]. This protein is found in several areas within cells, including the ER lumen, plasma membrane, intracellular space, and perinuclear region [ 102 ].…”

Section: Er Stress Mitochondrial Dysfunction and Inhibition Of Autoph...mentioning

confidence: 99%

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Recent Insights into the Biomarkers, Molecular Targets and Mechanisms of Non-Alcoholic Steatohepatitis-Driven Hepatocarcinogenesis

Kakehashi,

Suzuki,

Wanibuchi

2023

Cancers

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Non-alcoholic fatty liver disease (NAFLD) or metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (NASH) are chronic hepatic conditions leading to hepatocellular carcinoma (HCC) development. According to the recent “multiple-parallel-hits hypothesis”, NASH could be caused by abnormal metabolism, accumulation of lipids, mitochondrial dysfunction, and oxidative and endoplasmic reticulum stresses and is found in obese and non-obese patients. Recent translational research studies have discovered new proteins and signaling pathways that are involved not only in the development of NAFLD but also in its progression to NASH, cirrhosis, and HCC. Nevertheless, the mechanisms of HCC developing from precancerous lesions have not yet been fully elucidated. Now, it is of particular importance to start research focusing on the discovery of novel molecular pathways that mediate alterations in glucose and lipid metabolism, which leads to the development of liver steatosis. The role of mTOR signaling in NASH progression to HCC has recently attracted attention. The goals of this review are (1) to highlight recent research on novel genetic and protein contributions to NAFLD/NASH; (2) to investigate how recent scientific findings might outline the process that causes NASH-associated HCC; and (3) to explore the reliable biomarkers/targets of NAFLD/NASH-associated hepatocarcinogenesis.

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Section: Er Stress Mitochondrial Dysfunction and Inhibition Of Autoph...mentioning

confidence: 99%

“…[ [47][48][49] Cache domain-containing 1 (CACHD1) PERK, Wnt, Notch NASH-HCC diagnosis. STAM mice NASH model, Huh7, and HepG2.…”

Section: Gene/protein/metabolite Altered Pathway Model Function Type ...mentioning

confidence: 99%

Recent Insights into the Biomarkers, Molecular Targets and Mechanisms of Non-Alcoholic Steatohepatitis-Driven Hepatocarcinogenesis

Kakehashi,

Suzuki,

Wanibuchi

2023

Cancers

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“…Canopy FGF signaling regulator 2 (CNPY2) is a cytoplasmic secreted protein that is widely expressed in various tissues and organs, and is a member of the canopy family, which also includes CNPY1, 3 and 4. Recently, it has been demonstrated that CNPY2 is an angiogenic growth factor ( 15 ). CNPY2 has also been found to be abnormally highly expressed in ApoE -/- mice and oxidized low-density lipoprotein-stimulated mouse aortic endothelial cells.…”

Section: Introductionmentioning

confidence: 99%

CNPY2 governs PDGF‑BB‑treated vascular smooth muscle cell proliferation, migration and phenotypic transformation via the Akt/mTOR/GSK‑3β signaling pathway

Sun,

Wang,

et al. 2024

Exp Ther Med

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Phenotype switching of vascular smooth muscle cells (VSMCs) is a pathological process in various vascular diseases. Canopy FGF signaling regulator 2 (CNPY2) has previously been found to be abnormally expressed in ApoE -/- mice and aortic endothelial cells, indicating it may have an important role in vascular diseases. The present study aimed to determine the role and mechanism of CNPY2 in VSMC phenotype switching. Following stimulation with platelet-derived growth factor type BB (PDGF-BB), the expression of CNPY2 in VSMCs was detected using reverse transcription-quantitative PCR and western blot analysis. Subsequently, to explore the regulatory effects of CNPY2 on VSMCs, CNPY2 expression was knocked down by transfection with short hairpin RNA and cell viability, proliferation, migration and phenotypic transformation indicators were detected. Western blot analysis was also used to detect the phosphorylation of Akt/mTOR/GSK-3β pathway-associated proteins downstream of CNPY2. In addition, pretreatment with the Akt pathway activator SC79 was performed to further explore the regulatory mechanisms of CNPY2. The results revealed that CNPY2 expression was upregulated in PDGF-BB-stimulated VSMCs. In addition, the knockdown of CNPY2 inhibited PDGF-BB-induced VSMC hyperproliferation, cell cycle arrest, migration and phenotypic transformation, as well the activation of Akt/mTOR/GSK-3β pathway-associated proteins. Pretreatment with SC79 significantly reversed the inhibitory effects of CNPY2 knockdown on the proliferation, cell cycle arrest, migration and phenotypic transformation of the model cells. In summary, the present study indicates that CNPY2 regulates the abnormal proliferation, migration and phenotypic transformation of PDGF-BB-stimulated VSMCs via activation of the Akt/mTOR/GSK-3β signaling pathway.

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Progress in Research on CNPY2 in Diseases

Cited by 2 publications

References 74 publications

Recent Insights into the Biomarkers, Molecular Targets and Mechanisms of Non-Alcoholic Steatohepatitis-Driven Hepatocarcinogenesis

Recent Insights into the Biomarkers, Molecular Targets and Mechanisms of Non-Alcoholic Steatohepatitis-Driven Hepatocarcinogenesis

CNPY2 governs PDGF‑BB‑treated vascular smooth muscle cell proliferation, migration and phenotypic transformation via the Akt/mTOR/GSK‑3β signaling pathway

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