Characterization of LGALS3 (galectin-3) as a player in DNA damage response

Renato S. Carvalho, Vanessa C. Fernandes, Thales C. Nepomuceno, Deivid C. Rodrigues, Nicholas T. Woods, Guilherme Suarez-Kurtz, Roger Chammas, Alvaro N. Monteiro, Marcelo A. Carvalho

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

DNA damage repair (DDR) is an orchestrated process encompassing the injury detection to its complete resolution. DNA double-strand break lesions are repaired mainly by two distinct mechanisms: the error-free homologous recombination (HR) and the error-prone non-homologous end-joining. Galectin-3 (GAL3) is the unique member of the chimeric galectins subfamily and is reported to be involved in several cancer development and progression related events. Recently our group described a putative protein interaction between GAL3 and BARD1, the main partner of breast and ovarian cancer susceptibility gene product BRCA1, both involved in HR pathway. In this report we characterized GAL3/ BARD1 protein interaction and evaluated the role of GAL3 in DDR pathways using GAL3 silenced human cells exposed to different DNA damage agents. In the absence of GAL3 we observed a delayed DDR response activation, as well as a decrease in the G2/M cell cycle checkpoint arrest associated with HR pathway. Moreover, using a TAP-MS approach we also determined the protein interaction network of GAL3.

Original languageEnglish (US)
Pages (from-to)840-850
Number of pages11
JournalCancer Biology and Therapy
Volume15
Issue number7
DOIs
Publication statusPublished - Jul 2014

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Keywords

  • BARD1
  • BRCA1
  • Cancer
  • DNA damage
  • Galectin-3

ASJC Scopus subject areas

  • Molecular Medicine
  • Oncology
  • Pharmacology
  • Cancer Research

Cite this

Carvalho, R. S., Fernandes, V. C., Nepomuceno, T. C., Rodrigues, D. C., Woods, N. T., Suarez-Kurtz, G., ... Carvalho, M. A. (2014). Characterization of LGALS3 (galectin-3) as a player in DNA damage response. Cancer Biology and Therapy, 15(7), 840-850. https://doi.org/10.4161/cbt.28873