Evidence map›Paper›PMID 24755837›Full record

ArticleCancer biology & therapy2014

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

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.9field-weighted citation impact, top 27% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Article
  6. Galectin-8 Contributes to Human Trophoblast Cell Invasion.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 7 institutions in 4 countries.

Renato S CarvalhoInstituto 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.
Vanessa C FernandesInstituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil.
Thales C NepomucenoInstituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil.
Deivid C RodriguesInstituto de Biofísica Carlos Chagas Filho; Universidade Federal do Rio de Janeiro; Rio de Janeiro, Brazil.
Nicholas T WoodsCancer Epidemiology Program; H. Lee Moffitt Cancer Center & Research Institute; Tampa, FL USA.
Guilherme Suarez-KurtzPrograma de Farmacologia; Instituto Nacional de Câncer; Rio de Janeiro, Brazil.
Roger ChammasFaculdade de Medicina; Universidade de São Paulo; São Paulo, Brazil.
Alvaro N MonteiroCancer Epidemiology Program; H. Lee Moffitt Cancer Center & Research Institute; Tampa, FL USA.
Marcelo A CarvalhoInstituto Federal do Rio de Janeiro (IFRJ); Rio de Janeiro, Brazil; Programa de Farmacologia; Instituto Nacional de Câncer; Rio de Janeiro, Brazil.
Rio de Janeiro Federal Institute of Education, Science and Technology · BRHospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRInstituto de Biofísica Carlos Chagas FilhoInstituto Nacional del Cáncer · CLMoffitt Cancer Center · USUniversidade Federal do Rio de Janeiro · BRUniversity of Tampa · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
NCI NIH HHS P30 CA076292
6 · The paper itself

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.

Indexed as

DNA DamageDNA RepairAntineoplastic AgentsBlood ProteinsBRCA1 ProteinCarboplatinEtoposideG2 Phase Cell Cycle CheckpointsGalectin 3GalectinsGene SilencingHEK293 CellsHeLa CellsHumansMitomycinProtein Interaction MapsAntineoplastic AgentsBARD1 protein, humanBlood ProteinsBRCA1 ProteinCarboplatinEtoposideGalectin 3GalectinsLGALS3 protein, humanMitomycinTumor Suppressor ProteinsUbiquitin-Protein LigasesBARD1BRCA1cancerDNA damagegalectin-3

Identifiers

PMID24755837
PMCPMC4100985
OpenAlexW2031989725

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.