Researchers investigated the effects of bile acids on tissue factor activity and thrombin generation in hepatocytes and correlated these effects with activation of farnesoid X receptor-dependent signaling and apoptosis.
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Greimel, T., Jahnel, J., Pohl, S., Strini, T., Tischitz, M., Meier-Allard, N., Holasek, S., Meinel, K., Aguiriano-Moser, V., Zobel, J., Haidl, H., Gallistl, S., Panzitt, K., Wagner, M., & Schlagenhauf, A. (2021). Bile acid-induced tissue factor activity in hepatocytes correlates with activation of farnesoid X receptor. Laboratory Investigation, 1–9. https://doi.org/10.1038/s41374-021-00628-z Cite
Using next-generation and Sanger sequencing investigators found that, p53 in Hep3B cells was impaired by TP53-FXR2 fusion, and that overexpression of the C19MC miRNA-520G in Hep3B cells promoted the expression of MAGEA-3, 6 and 12 mRNAs.
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Jinesh, G. G., Napoli, M., Smallin, M. T., Davis, A., Ackerman, H. D., Raulji, P., Montey, N., Flores, E. R., & Brohl, A. S. (2021). Mutant p53s and chromosome 19 microRNA cluster overexpression regulate cancer testis antigen expression and cellular transformation in hepatocellular carcinoma. Scientific Reports, 11(1), 12673. https://doi.org/10.1038/s41598-021-91924-7 Cite
Scientists discuss how anti-fibrotic therapies have progressed over the years, and how nanomedicine formulations can potentiate anti-fibrotic treatment efficacy.
[Advanced Drug Delivery Reviews]
The authors summarize the formation strategies and a wide range of applications in biomedicine of liver organoid.
[Tissue Engineering and Regenerative Medicine]
Buried in a bill approved by the US Senate to help the United States compete with China is language that is drawing fire from human genome researchers. It would require the NIH to develop new security protocols aimed at preventing the misuse of US-funded genomic data by China and other nations.
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In addition to hepatocytes, several hepsin-producing prostate cancer cell lines showed reduced STING-mediated type I interferon induction and responses.
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Gilead Sciences, Inc. announced that the US FDA has approved an expansion of the pediatric indication of Epclusa® for the treatment of chronic hepatitis C virus (HCV) to now include children as young as 3 years of age, regardless of HCV genotype or liver disease severity.
[Gilead Sciences, Inc.]
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Scientists showed that the branched-chain fatty acids, isobutyric and isovaleric acid, increased glucose production and activated mTORC1/S6K1 in hepatocytes.
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Choi, B. S.-Y., Daniel, N., Houde, V. P., Ouellette, A., Marcotte, B., Varin, T. V., Vors, C., Feutry, P., Ilkayeva, O., Ståhlman, M., St-Pierre, P., Bäckhed, F., Tremblay, A., White, P. J., & Marette, A. (2021). Feeding diversified protein sources exacerbates hepatic insulin resistance via increased gut microbial branched-chain fatty acids and mTORC1 signaling in obese mice. Nature Communications, 12(1), 3377. https://doi.org/10.1038/s41467-021-23782-w Cite
Researchers reported a new factor, CDCA2, in promoting hepatocellular carcinoma (HCC) development. CDCA2 amplification was reported as an independent risk factor for the recurrence and survival of HCC patients, which was positively correlated with elevated level of alpha-fetoprotein, high histological grade, large tumor size, advanced TNM stage, and poor prognosis for HCC patients.
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Scientists explored the role of CPSF4, for 3′ end formation and cleavage, in circRNA formation. Clinical research had shown that CPSF4 expression was upregulated in hepatocellular carcinoma (HCC) and that high expression of CPSF4 was associated with poor prognosis in HCC patients.
Gain or loss-of-function studies indicated that the reduction of CircC16orf62 expression promoted the proliferation, invasion, and glycolysis of hepatocellular carcinoma in vitro and in vivo.
[Cell Death & Disease]
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Zhang, S., Lu, Y., Jiang, H.-Y., Cheng, Z.-M., Wei, Z.-J., Wei, Y.-H., Liu, T., Xia, B.-J., Zhao, X.-Y., Huang, Y., Zou, X., Liu, R., & Zhou, S. (2021). CircC16orf62 promotes hepatocellular carcinoma progression through the miR-138-5p/PTK2/AKT axis. Cell Death & Disease, 12(6), 1–13. https://doi.org/10.1038/s41419-021-03866-7 Cite