NDLI: Fluvastatin Interferes with Hepatitis C Virus Replication via Microtubule Bundling and a Doublecortin-like Kinase-Mediated Mechanism

Content Provider	PubMed Central
Author	Ali, Naushad Allam, Heba Bader, Ted May, Randal Basalingappa, Kanthesh M. Berry, William L. Parthasarathy, Chandrakesan Qu, Dongfeng Nathaniel, Weygant Bronze, Michael S. Umar, Shahid Ralf, Janknecht Sureban, Sripathi M. Mark, Huycke Houchen, Courtney W.
Editor	Waris, Gulam
Copyright Year	2013
Abstract	Hepatitis C virus (HCV)-induced alterations in lipid metabolism and cellular protein expression contribute to viral pathogenesis. The mechanism of pleiotropic actions of cholesterol-lowering drugs, statins, against HCV and multiple cancers are not well understood. We investigated effects of fluvastatin (FLV) on microtubule-associated and cancer stem cell marker (CSC), doublecortin-like kinase 1 (DCLK1) during HCV-induced hepatocarcinogenesis. HCV replication models, cancer cell lines and normal human hepatocytes were used to investigate the antiviral and antitumor effects of statins. FLV treatment resulted in induction of microtubule bundling, cell-cycle arrest and alterations in cellular DCLK1 distribution in HCV-expressing hepatoma cells. These events adversely affected the survival of liver-derived tumor cells without affecting normal human hepatocytes. FLV downregulated HCV replication in cell culture where the ATP pool and cell viability were not compromised. Pravastatin did not exhibit these effects on HCV replication, microtubules and cancer cells. The levels of miR-122 that regulates liver homeostasis and provides HCV genomic stability remained at steady state whereas DCLK1 mRNA levels were considerably reduced during FLV treatment. We further demonstrated that HCV replication was increased with DCLK1 overexpression. In conclusion, unique effects of FLV on microtubules and their binding partner DCLK1 are likely to contribute to its anti-HCV and antitumor activities in addition to its known inhibitory effects on 3-hydroxy-3-methylglutary-CoA reductase (HMGCR).
Related Links	http://dx.doi.org/10.1371/journal.pone.0080304
Starting Page	80304
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	11
Volume Number	8
Language	English
Publisher	Public Library of Science
Publisher Date	2013-11-19
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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Correction: Fluvastatin Interferes with Hepatitis C Virus Replication via Microtubule Bundling and a Doublecortin-like Kinase-Mediated Mechanism

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Fluvastatin Interferes with Hepatitis C Virus Replication via Microtubule Bundling and a Doublecortin-like Kinase-Mediated Mechanism

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Correction: Fluvastatin Interferes with Hepatitis C Virus Replication via Microtubule Bundling and a Doublecortin-like Kinase-Mediated Mechanism

Enhanced hepatitis C virus genome replication and lipid accumulation mediated by inhibition of AMP-activated protein kinase

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Hepatitis C Virus Core-Derived Peptides Inhibit Genotype 1b Viral Genome Replication via Interaction with DDX3X

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Fluvastatin Interferes with Hepatitis C Virus Replication via Microtubule Bundling and a Doublecortin-like Kinase-Mediated Mechanism