Loss of fragile histidine triad (Fhit) protein expression alters the translation of cancer-associated mRNAs

Daniel L. Kiss, William D. Baez, Kay Huebner, Ralf Bundschuh, Daniel R. Schoenberg

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Objectives: In > 50% of cancers tumor development involves the early loss of Fhit (fragile histidine triad) protein expression, yet the mechanistic pathway(s) by which Fhit mediates its tumor suppressor functions are not fully understood. Earlier attempts to identify a Fhit-deficient gene expression profile relied on total cellular RNA and microarray analysis. The data here used RNA sequencing (RNA-Seq) of Fhit-negative and Fhit-positive cells as proof of principle for the impact of Fhit on specific mRNAs, and to lay the foundation for a study using ribosome profiling to identify mRNAs whose translation is affected by FHIT loss. Data description: RNA-Seq was performed on RNA from lines of Fhit-expressing and Fhit-deficient lung cancer cells. This identified changes in the levels of mRNAs for a number of cell survival and cell cycle progression genes. Polysome profile analysis performed on cytoplasmic extracts from Fhit-negative and Fhit-positive cells showed changes in the sedimentation of select mRNAs consistent with changes in translation efficiency. The impact of differential Fhit expression on the turnover of selected cancer-linked mRNAs was determined by RT-qPCR of cytoplasmic RNA isolated at intervals after treating cells with a transcription inhibitor.

Original languageEnglish (US)
Article number178
JournalBMC Research Notes
Volume11
Issue number1
DOIs
StatePublished - Mar 14 2018

Keywords

  • Cancer
  • Fhit
  • Polysome gradients
  • Translational control
  • Tumor suppressor
  • mRNA sequencing

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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