Recombinant viral capsid protein VP1 suppresses migration and invasion of human cervical cancer by modulating phosphorylated prohibitin in lipid rafts

Ching Feng Chiu, Jei Ming Peng, Shao Wen Hung, Chi Ming Liang, Shu Mei Liang

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Recombinant capsid protein VP1 (rVP1) of foot-and-mouth disease virus inhibits invasion/metastasis of cancer cells. Here we studied its mechanism of action on human cervical cancer cells. The inhibition of cell invasion by rVP1 was accompanied with reduction in phosphatidylinositol (3,4,5)-triphosphate (PIP3), phospho-Akt S473, phosphorylated prohibitin (phospho-PHB) T258 in lipid rafts, dissociation of phospho-PHB T258 with Raf-1 and the inactivation of Raf-1/ERK. Addition of PIP3 or overexpression of constitutively active Akt and raft-anchored PHB T258 but not PHB T258I mutant protein reversed the inhibitory effects of rVP1. rVP1 inhibited cervical tumor growth and metastasis, and prolonged survival in xenograft mouse models. These results suggest that rVP1 inhibits cancer metastasis via de-phosphorylation of Akt and PHB T258 in lipid rafts to downregulate Raf/ERK signaling.

Original languageEnglish
Pages (from-to)205-214
Number of pages10
JournalCancer Letters
Volume320
Issue number2
DOIs
Publication statusPublished - Jul 28 2012
Externally publishedYes

Fingerprint

Capsid Proteins
Viral Proteins
Recombinant Proteins
Uterine Cervical Neoplasms
Neoplasm Metastasis
Lipids
Foot-and-Mouth Disease Virus
Neoplasms
Mutant Proteins
Heterografts
Down-Regulation
Phosphorylation
Survival
Growth
prohibitin

Keywords

  • Cancer metastasis
  • PIP3
  • Prohibitin
  • Raf-1
  • RVP1

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Recombinant viral capsid protein VP1 suppresses migration and invasion of human cervical cancer by modulating phosphorylated prohibitin in lipid rafts. / Chiu, Ching Feng; Peng, Jei Ming; Hung, Shao Wen; Liang, Chi Ming; Liang, Shu Mei.

In: Cancer Letters, Vol. 320, No. 2, 28.07.2012, p. 205-214.

Research output: Contribution to journalArticle

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