title: Characterization of LGALS3 (galectin-3) as a player in DNA damage response.
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 G 2/M cell cycle checkpoint arrest associated with HR pathway. Moreover, using a TAP-MS approach we also determined the protein interaction network of GAL3.
authors.affiliation: Instituto de Biofísica Carlos Chagas Filho; Universidade Federal do Rio de Janeiro; Rio de Janeiro, Brazil; Cancer Epidemiology Program; H. Lee Moffitt Cancer Center & Research Institute; Tampa, FL USA.
authors.forename: Renato S
authors.initials: RS
authors.lastname: Carvalho
authors.affiliation: Instituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil.
authors.forename: Vanessa C
authors.initials: VC
authors.lastname: Fernandes
authors.affiliation: Instituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil.
authors.forename: Thales C
authors.initials: TC
authors.lastname: Nepomuceno
authors.affiliation: Instituto de Biofísica Carlos Chagas Filho; Universidade Federal do Rio de Janeiro; Rio de Janeiro, Brazil.
authors.forename: Deivid C
authors.initials: DC
authors.lastname: Rodrigues
authors.affiliation: Cancer Epidemiology Program; H. Lee Moffitt Cancer Center & Research Institute; Tampa, FL USA.
authors.forename: Nicholas T
authors.initials: NT
authors.lastname: Woods
authors.affiliation: Programa de Farmacologia; Instituto Nacional de Câncer; Rio de Janeiro, Brazil.
authors.forename: Guilherme
authors.initials: G
authors.lastname: Suarez-Kurtz
authors.affiliation: Faculdade de Medicina; Universidade de São Paulo; São Paulo, Brazil.
authors.forename: Roger
authors.initials: R
authors.lastname: Chammas
authors.affiliation: Cancer Epidemiology Program; H. Lee Moffitt Cancer Center & Research Institute; Tampa, FL USA.
authors.forename: Alvaro N
authors.initials: AN
authors.lastname: Monteiro
authors.affiliation: Instituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil; Programa de Farmacologia; Instituto Nacional de Câncer; Rio de Janeiro, Brazil.
authors.forename: Marcelo A
authors.initials: MA
authors.lastname: Carvalho
mesh_terms: D000970:Antineoplastic Agents / Q000494:pharmacology; D019313:BRCA1 Protein / Q000378:metabolism; D001798:Blood Proteins; D016190:Carboplatin / Q000494:pharmacology; D004249:DNA Damage; D004260:DNA Repair; D005047:Etoposide / Q000494:pharmacology; D059565:G2 Phase Cell Cycle Checkpoints; D037502:Galectin 3 / Q000235:genetics / Q000378:metabolism*; D037161:Galectins; D020868:Gene Silencing; D057809:HEK293 Cells; D006367:HeLa Cells; D006801:Humans; D016685:Mitomycin / Q000494:pharmacology; D060066:Protein Interaction Maps; D015398:Signal Transduction; D025521:Tumor Suppressor Proteins / Q000378:metabolism; D044767:Ubiquitin-Protein Ligases / Q000378:metabolism; D054875:Ubiquitination
chemical_list: D000970:Antineoplastic Agents; D019313:BRCA1 Protein; D001798:Blood Proteins; D037502:Galectin 3; D037161:Galectins; C428445:LGALS3 protein, human; D025521:Tumor Suppressor Proteins; D016685:Mitomycin; D005047:Etoposide; D016190:Carboplatin; C102449:BARD1 protein, human; D044767:Ubiquitin-Protein Ligases
keywords: BARD1; BRCA1; DNA damage; cancer; galectin-3
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