Subcutaneous and intrahepatic growth of human hepatoblastoma in immunodeficient mice

Schnater, J. Marco; Bruder, Elisabeth; Bertschin, S.; Woodtli, Thomas; Theije, Chiel de; Pietsch, Torsten; Aronson, Daniël C.; Schweinitz, Dietrich von; Lamers, Wouter H.; Köhler, S. Eleonore

doi:10.1016/j.jhep.2006.03.018

Cited by 34 publications

(37 citation statements)

References 40 publications

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“…Within this time window, macroscopic metastases were not observed in livers and lungs. It should be noted that in previous studies, even longer tests were insufficient to observe HepG2 metastasis [52]. HepG2 tumors also showed minimal local invasion, albeit in the macadamia-treated group we observed one anecdotal tumor invading the adjacent muscles.…”

Section: Discussioncontrasting

confidence: 56%

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

Vinciguerra

Carrozzino

Peyrou

et al. 2009

Journal of Hepatology

114

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Section: Discussioncontrasting

confidence: 56%

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

Vinciguerra

Carrozzino

Peyrou

et al. 2009

Journal of Hepatology

114

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“…Moreover, these cells display a longer doubling time than Huh6 cells (compare left and right panels in Fig. 4B) 25. Beta‐catenin is the main effector of the Wnt signaling pathway and induces the transcription of numerous oncogenes, such as CCND1 or MYC , when associated with its transcriptional partner transcription factor 4 (TCF4).…”

Section: Resultsmentioning

confidence: 95%

MicroRNA therapy inhibits hepatoblastoma growth in vivo by targeting β‐catenin and Wnt signaling

Indersie

Lesjean

Hooks

et al. 2017

Hepatology Communications

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Hepatoblastoma (HBL) is the most common pediatric liver cancer. In this malignant neoplasm, beta‐catenin protein accumulates and increases Wnt signaling due to recurrent activating mutations in the catenin‐beta 1 (CTNNB1) gene. Therefore, beta‐catenin is a key therapeutic target in HBL. However, controlling beta‐catenin production with therapeutic molecules has been challenging. New biological studies could provide alternative therapeutic solutions for the treatment of HBL, especially for advanced tumors and metastatic disease. In this study, we identified microRNAs (miRNAs) that target beta‐catenin and block HBL cell proliferation in vitro and tumor growth in vivo. Using our dual‐fluorescence‐FunREG system, we screened a library of 1,712 miRNA mimics and selected candidates inhibiting CTNNB1 expression through interaction with its untranslated regions. After validating the regulatory effect of nine miRNAs on beta‐catenin in HBL cells, we measured their expression in patient samples. Let‐7i‐3p, miR‐449b‐3p, miR‐624‐5p, and miR‐885‐5p were decreased in tumors compared to normal livers. Moreover, they inhibited HBL cell growth and Wnt signaling activity in vitro partly through beta‐catenin down‐regulation. Additionally, miR‐624‐5p induced cell senescence in vitro, blocked experimental HBL growth in vivo, and directly targeted the beta‐catenin 3′‐untranslated region. Conclusion: Our results shed light on how beta‐catenin‐regulating miRNAs control HBL progression through Wnt signaling inactivation. In particular, miR‐624‐5p may constitute a promising candidate for miRNA replacement therapy for HBL patients. (Hepatology Communications 2017;1:168‐183)

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“…It is often used as the serum marker of fetal defects and tumors to diagnose disease and to monitor disease progression. AFP can perform a lot of important physiological functions, including binding to and transferring numerous receptors (e.g., bilirubin, drugs), maintaining plasma colloid osmotic pressure (Gillespie and Uversky, 2000), performing bilateral regulatory functions as a growth regulatory factor (Li et al, 2002;Dudich et al, 2006;Oertel et al, 2006;Schnater et al, 2006), serving as a sensitive serum marker of primary liver cancer (Leerapun et al, 2007;Montaser et al, 2007), playing a role in the diagnosis of fetal defects or neonatal diseases (Dashe et al, 2006;Odibo et al, 2006;Rozenberg et al, 2006;Wald et al, 2006), and serving as a prognostic marker of acute hepatic failure (Amemiya et al, 2004;Butterfield, 2007). Therefore, AFP may play a positive role in the treatment of hepatic failure.…”

Section: Discussionmentioning

confidence: 99%

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

Chang¹,

You²,

Liu³

et al. 2014

Genet. Mol. Res.

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ABSTRACT. This study aimed to enhance the drug metabolism function of the human hepatoma cell line C3A and to explore the related significance for patients with severe liver disease. The important liver phase I and phase II drug metabolism enzymes, cytochrome P450 3A4 (CYP 3A4) and glutathione S-transferase A1 (GST A1), were constructed into a double expression vector and then transfected into C3A cells. Furthermore, in order to increase the expression of CYP 3A4 and GST A1, they were optimized according to human optimal codons. Another double-expression vector, pBudCE4.1-optimized CYP 3A4-optimized GST A1, was constructed and then transfected into C3A to establish a stable cell line. The drug metabolism function of C3A was evaluated. Sequence determination and analysis results showed that the recombinant plasmid pBudCE4.1-CYP 3A4-GST A1 met the application standard and its transfection was successful. The expression and activity of CYP 3A4 and GST A1 in unoptimized C3A cells were higher than those in blank C3A cells. Unoptimized C3A had a better drug metabolism function. Although some C3A cells transfected with pBudCE4.1-optimized CYP 3A4-optimized GST A1 survived, they grew slowly, and were therefore not applicable in clinical practice. Unoptimized C3A is superior to blank C3A in drug metabolism, and could be applied in the bioartificial liver support system as a new material.

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Subcutaneous and intrahepatic growth of human hepatoblastoma in immunodeficient mice

Cited by 34 publications

References 40 publications

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

Unsaturated fatty acids promote hepatoma proliferation and progression through downregulation of the tumor suppressor PTEN

MicroRNA therapy inhibits hepatoblastoma growth in vivo by targeting β‐catenin and Wnt signaling

Establishment of cytochrome P450 3A4 and glutathione S-transferase A1-transfected human hepatoma cell line and functional analysis

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