Hepatitis B virus X protein disrupts stress fiber formation and triggers apoptosis

Chan Yen Kuo, Tzu Yu Chou, Chun Ming Chen, Yung Fong Tsai, Guang Yuh Hwang, Tsong Long Hwang*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

11 Scopus citations

Abstract

Cytoskeletal proteins are key participants in the cellular progression to apoptosis. In a previous study we injected nude mice with CCL13-HBx cells and identified in contrast to non-HBx transfected cells a differentially phosphorylated myosin light chain (p-MLC) by two-dimensional PAGE and mass spectrometry of the tumor material. To investigate the role of HBx in myosin light chain kinase (MLCK) signaling pathways, we analyzed the key molecules, p-MLC and MLCK, by western blotting. Immunofluorescence staining analysis showed that HBx disrupted stress fiber formation and that focal adhesion kinase (FAK) and integrin-linked kinase (ILK) were regulated by HBx-mediated phosphatase and tensin homolog (PTEN). We also used pharmacological inhibitors to explore the correlation between cytoskeletal rearrangements and HBx-mediated cell apoptosis via an MLCK and a PTEN-dependent pathway. The results showed that both ML9 and bvp restored the effects caused by HBx induction. Our findings suggest that HBx disrupts stress fiber formation and triggers apoptosis via an MLCK and a PTEN-dependent pathway.

Original languageEnglish
Pages (from-to)20-29
Number of pages10
JournalVirus Research
Volume175
Issue number1
DOIs
StatePublished - 07 2013

Keywords

  • Apoptosis
  • HBx
  • MLCK
  • PTEN
  • Stress-fiber formation

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