Evidence map›Paper›PMID 38832821›Full record

ArticleRNA biology2024

Decoding LINC00052 role in breast cancer by bioinformatic and experimental analyses.

Jose Manuel Sanchez-Lopez, Miguel Angel Juarez-Mancera, Benjamin Bustamante, Araceli Ruiz-Silvestre, Magali Espinosa, Gretel Mendoza-Almanza, Gisela Ceballos-Cancino, Jorge Melendez-Zajgla, Vilma Maldonado, Floria Lizarraga

Abstract read
In one paragraph

Article in RNA biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
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

10 authors.

Jose Manuel Sanchez-LopezLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Miguel Angel Juarez-ManceraLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Benjamin BustamanteLaboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Araceli Ruiz-SilvestreLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Magali EspinosaLaboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Gretel Mendoza-AlmanzaLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Gisela Ceballos-CancinoLaboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Jorge Melendez-ZajglaLaboratorio de Genomica Funcional del Cancer, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Vilma MaldonadoLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.
Floria LizarragaLaboratorio de Epigenetica, Instituto Nacional de Medicina Genomica (INMEGEN), Ciudad de México, Mexico.ORCID 0000-0001-8756-405X

Funding

Consejo Nacional de Ciencia y Tecnología 777479Consejo Nacional de Ciencia y Tecnología FORDECYT-PRONACES/6657/2020
6 · The paper itself

Abstract

LncRNA is a group of transcripts with a length exceeding 200 nucleotides that contribute to tumour development. Our research group found that LINC00052 expression was repressed during the formation of breast cancer (BC) multicellular spheroids. Intriguingly, LINC00052 precise role in BC remains uncertain. We explored LINC00052 expression in BC patients` RNA samples (TCGA) in silico, as well as in an in-house patient cohort, and inferred its cellular and molecular mechanisms. In vitro studies evaluated LINC00052 relevance in BC cells viability, cell cycle and DNA damage. Results. Bioinformatic RNAseq analysis of BC patients showed that LINC00052 is overexpressed in samples from all BC molecular subtypes. A similar LINC00052 expression pattern was observed in an in-house patient cohort. In addition, higher LINC00052 levels are related to better BC patient´s overall survival. Remarkably, MCF-7 and ZR-75-1 cells treated with estradiol showed increased LINC00052 expression compared to control, while these changes were not observed in MDA-MB-231 cells. In parallel, bioinformatic analyses indicated that LINC00052 influences DNA damage and cell cycle. MCF-7 cells with low LINC00052 levels exhibited increased cellular protection against DNA damage and diminished growth capacity. Furthermore, in cisplatin-resistant MCF-7 cells, LINC00052 expression was downregulated. Conclusion. This work shows that LINC00052 expression is associated with better BC patient survival. Remarkably, LINC00052 expression can be regulated by Estradiol. Additionally, assays suggest that LINC00052 could modulate MCF-7 cells growth and DNA damage repair. Overall, this study highlights the need for further research to unravel LINC00052 molecular mechanisms and potential clinical applications in BC.

Indexed as

Breast NeoplasmsGene Expression Regulation, NeoplasticRNA, Long NoncodingBiomarkers, TumorCell CycleCell Line, TumorCell ProliferationCell SurvivalComputational BiologyDNA DamageDrug Resistance, NeoplasmFemaleGene Expression ProfilingHumansMCF-7 CellsPrognosisBiomarkers, TumorRNA, Long Noncodingbreast cancerDNA damageEstrogen receptorLINC00052lncRNA

Identifiers

PMID38832821
PMCPMC11152094

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Registered trials

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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.