The Emerging Roles of Cancer Stem Cells and Wnt/Beta-Catenin Signaling in Hepatoblastoma

Mavila, Nirmala; Thundimadathil, Jyothi

doi:10.3390/cancers11101406

Cited by 36 publications

(31 citation statements)

References 89 publications

(115 reference statements)

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“…Members of the classical pathway include the extracellular Wnt factor, transmembrane receptor, β-catenin, glycogen synthase kinase-3β (GSK3β), adenomatous polyposis coli (APC), Axin, and casein kinase-1 (CK1) ( 10 , 80 ). When the classical Wnt pathway is unactivated, GSK3β in the cytoplasm can phosphorylate β-catenin in the form of a complex with APC, Axin, and CK1 ( 81 ). By recognition of the phosphorylation site of β-catenin, β-TrCP can ubiquitinate β-catenin, then degrade it through a proteasome, and maintain a low level of β-catenin in cells ( 82 ).…”

Section: Molecular Mechanisms Of Change In Biological Behaviormentioning

confidence: 99%

Molecular Mechanism and Approach in Progression of Meningioma

et al. 2020

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Meningioma is the most common tumor of the central nervous system, most of which is benign. Even after complete resection, a high rate of recurrence of meningioma is observed. From in-depth study of its pathogenesis, it has been found that a number of chromosomal variations and abnormal molecular signals are closely related to the occurrence and development of malignancy in meningioma, which may provide the theoretical basis and potential direction for accurate and targeted treatment. We have reviewed advances in chromosomal variations and molecular mechanisms involved in the progression of meningioma, and have highlighted the association with malignant biological behavior including cell proliferation, angiogenesis, increased invasiveness, and inhibition of apoptosis. In addition, the chemotherapy of meningioma is summarized and discussed.

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Section: Molecular Mechanisms Of Change In Biological Behaviormentioning

confidence: 99%

Molecular Mechanism and Approach in Progression of Meningioma

et al. 2020

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“…Liver cancer is the seventh most commonly diagnosed cancer and the third leading cause of cancer death worldwide, and mainly includes hepatocellular carcinoma, cholangiocarcinoma and hepatoblastoma 1 , 2 . Hepatoblastoma is the most common malignant hepatic tumor in pediatrics and is considered to originate from hepatoblasts or embryonic liver progenitor cells 3 . The HepG2 cell line was originally isolated from primary hepatoblastoma of a 15-year-old Caucasian male, and exhibits epithelial-like morphology 4 – 6 .…”

Section: Introductionmentioning

confidence: 99%

Alterations in cellular and organellar phospholipid compositions of HepG2 cells during cell growth

Tsuji

Morita

Nakamura

et al. 2021

Sci Rep

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The human hepatoblastoma cell line, HepG2, has been used for investigating a wide variety of physiological and pathophysiological processes. However, less information is available about the phospholipid metabolism in HepG2 cells. In the present report, to clarify the relationship between cell growth and phospholipid metabolism in HepG2 cells, we examined the phospholipid class compositions of the cells and their intracellular organelles by using enzymatic fluorometric methods. In HepG2 cells, the ratios of all phospholipid classes, but not the ratio of cholesterol, markedly changed with cell growth. Of note, depending on cell growth, the phosphatidic acid (PA) ratio increased and phosphatidylcholine (PC) ratio decreased in the nuclear membranes, the sphingomyelin (SM) ratio increased in the microsomal membranes, and the phosphatidylethanolamine (PE) ratio increased and the phosphatidylserine (PS) ratio decreased in the mitochondrial membranes. Moreover, the mRNA expression levels of enzymes related to PC, PE, PS, PA, SM and cardiolipin syntheses changed during cell growth. We suggest that the phospholipid class compositions of organellar membranes are tightly regulated by cell growth. These findings provide a basis for future investigations of cancer cell growth and lipid metabolism.

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“…Hepatoblastoma (HB) is the most common primary malignant tumor of the liver in children, accounting for 80% of pediatric hepatic malignancies and 1% of all malignant tumors in children, with an increasing trend in recent years. 1 , 2 , 3 , 4 , 5 HB is an embryonal tumor, and overactivation of Wnt/β-catenin, hedgehog, and phosphatidylinositol 3-kinase (PI3K)/Akt signaling has been reported to be associated with its development. 5 , 6 , 7 , 8 , 9 Recent progress in research and development of comprehensive treatments has significantly improved the prognosis of HB.…”

Section: Introductionmentioning

confidence: 99%

“… 1 , 2 , 3 , 4 , 5 HB is an embryonal tumor, and overactivation of Wnt/β-catenin, hedgehog, and phosphatidylinositol 3-kinase (PI3K)/Akt signaling has been reported to be associated with its development. 5 , 6 , 7 , 8 , 9 Recent progress in research and development of comprehensive treatments has significantly improved the prognosis of HB. 4 , 5 , 10 , 11 , 12 , 13 , 14 However, high-risk HB, especially in patients with extrahepatic involvement, multifocal lesions, or distant metastases, still has a poor prognosis.…”

Section: Introductionmentioning

confidence: 99%

“… 5 , 6 , 7 , 8 , 9 Recent progress in research and development of comprehensive treatments has significantly improved the prognosis of HB. 4 , 5 , 10 , 11 , 12 , 13 , 14 However, high-risk HB, especially in patients with extrahepatic involvement, multifocal lesions, or distant metastases, still has a poor prognosis. 15 , 16 , 17 , 18 , 19 Present studies on molecular-targeted drugs are thus in progress with the aim of improving the prognosis for children with high-risk HB.…”

Section: Introductionmentioning

confidence: 99%

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S119N Mutation of the E3 Ubiquitin Ligase SPOP Suppresses SLC7A1 Degradation to Regulate Hepatoblastoma Progression

Zhang

Liu

et al. 2020

Molecular Therapy - Oncolytics

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A previous study on hepatoblastoma revealed novel mutations and cancer genes in the Wnt pathway and ubiquitin ligase complex, including the tumor suppressor speckle-type BTB/POZ (SPOP). Moreover, the SPOP gene affected cell growth, and its S119N mutation was identified as a loss-of-function mutation in hepatoblastoma. This study aimed to explore more functions and the potential mechanism of SPOP and its S119N mutation. The in vitro effects of SPOP on cell proliferation, invasion, apoptosis, and in vivo tumor growth were investigated by western blot analysis, Cell Counting Kit-8, colony formation assay, flow cytometry, and xenograft animal experiments. The substrate of SPOP was discovered by a protein quantification assay and quantitative ubiquitination modification assay. The present study further proved that SPOP functioned as an anti-oncogene through the phosphatidylinositol 3-kinase/Akt signaling pathway to affect various malignant biological behaviors of hepatoblastoma both in vitro and in vivo . Furthermore, experimental results also suggested that solute carrier family 7 member 1 (SLC7A1) might be a substrate of SPOP and influence cell phenotype by regulating arginine metabolism. In conclusion, these findings demonstrated the function of SPOP and revealed a potential substrate related to hepatoblastoma tumorigenesis, which might thus provide a novel therapeutic target for hepatoblastoma.

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The Emerging Roles of Cancer Stem Cells and Wnt/Beta-Catenin Signaling in Hepatoblastoma

Cited by 36 publications

References 89 publications

Molecular Mechanism and Approach in Progression of Meningioma

Molecular Mechanism and Approach in Progression of Meningioma

Alterations in cellular and organellar phospholipid compositions of HepG2 cells during cell growth

S119N Mutation of the E3 Ubiquitin Ligase SPOP Suppresses SLC7A1 Degradation to Regulate Hepatoblastoma Progression

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