Evidence map›Paper›PMID 26372729›Full record

ArticleOncotarget2015

BCAT1 expression associates with ovarian cancer progression: possible implications in altered disease metabolism.

Zhi-Qiang Wang, Adnen Faddaoui, Magdalena Bachvarova, Marie Plante, Jean Gregoire, Marie-Claude Renaud, Alexandra Sebastianelli, Chantal Guillemette, Stéphane Gobeil, Elizabeth Macdonald and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 9% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

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10 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 1 country.

Zhi-Qiang WangDepartment of Molecular Medicine, Laval University, Québec PQ, Canada.
Adnen FaddaouiDepartment of Molecular Medicine, Laval University, Québec PQ, Canada.
Magdalena BachvarovaCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec PQ, Canada.
Marie PlanteCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec PQ, Canada.
Jean GregoireCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec PQ, Canada.
Marie-Claude RenaudCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec PQ, Canada.
Alexandra SebastianelliCentre de recherche du CHU de Québec, L'Hôtel-Dieu de Québec, Québec PQ, Canada.
Chantal GuillemetteCentre de recherche du CHU de Québec, CHUL, Québec PQ, Canada.
Stéphane GobeilDepartment of Molecular Medicine, Laval University, Québec PQ, Canada.
Elizabeth MacdonaldDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Barbara VanderhydenDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.
Dimcho BachvarovDepartment of Molecular Medicine, Laval University, Québec PQ, Canada.
Hôtel-Dieu de Québec · CAUniversité Laval · CAUniversity of Ottawa · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously, we have identified the branched chain amino-acid transaminase 1 (BCAT1) gene as notably hypomethylated in low-malignant potential (LMP) and high-grade (HG) serous epithelial ovarian tumors, compared to normal ovarian tissues. Here we show that BCAT1 is strongly overexpressed in both LMP and HG serous epithelial ovarian tumors, which probably correlates with its hypomethylated status. Knockdown of the BCAT1 expression in epithelial ovarian cancer (EOC) cells led to sharp decrease of cell proliferation, migration and invasion and inhibited cell cycle progression. BCAT1 silencing was associated with the suppression of numerous genes and pathways known previously to be implicated in ovarian tumorigenesis, and the induction of some tumor suppressor genes (TSGs). Moreover, BCAT1 suppression resulted in downregulation of numerous genes implicated in lipid production and protein synthesis, suggesting its important role in controlling EOC metabolism. Further metabolomic analyses were indicative for significant depletion of most amino acids and different phospho- and sphingolipids following BCAT1 knockdown. Finally, BCAT1 suppression led to significantly prolonged survival time in xenograft model of advanced peritoneal EOC. Taken together, our findings provide new insights about the functional role of BCAT1 in ovarian carcinogenesis and identify this transaminase as a novel EOC biomarker and putative EOC therapeutic target.

Indexed as

MetabolomicsAgedAnimalsApoptosisBlotting, WesternCarcinoma, Ovarian EpithelialCell ProliferationFemaleFollow-Up StudiesGene Expression ProfilingHumansImmunoenzyme TechniquesMice, SCIDNeoplasm GradingNeoplasms, Glandular and EpithelialNeoplasm StagingBCAT1 protein, humanRNA, Small InterferingTransaminasesBCAT1cancer metabolismDNA hypomethylationmetastasisovarian cancer

Identifiers

PMID26372729
PMCPMC4741622
OpenAlexW2186508115

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.