Evidence map›Paper›PMID 32839509›Full record

ArticleScientific reports2020

FAM83H-AS1 is a potential modulator of cancer driver genes across different tumors and a prognostic marker for ER/PR + BRCA patients.

Magdalena Ríos-Romero, Alberto Cedro-Tanda, Mónica Peña-Luna, Marco Antonio Mancera-Rodríguez, Lizbett Hidalgo-Pérez, Mireya Cisneros-Villanueva, Fredy Omar Beltrán-Anaya, Rocío Arellano-Llamas, Silvia Jiménez-Morales, Luis Alberto Alfaro-Ruíz and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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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

15 authors at 1 institution in 1 country.

Magdalena Ríos-RomeroLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Alberto Cedro-TandaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.ORCID http://orcid.org/0000-0001-8708-462X
Mónica Peña-LunaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Marco Antonio Mancera-RodríguezLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Lizbett Hidalgo-PérezLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Mireya Cisneros-VillanuevaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Fredy Omar Beltrán-AnayaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.ORCID http://orcid.org/0000-0001-6862-7879
Rocío Arellano-LlamasLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Silvia Jiménez-MoralesLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Luis Alberto Alfaro-RuízLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Alberto Tenorio-TorresFundación de Cáncer de Mama, FUCAM, Ciudad de México, Mexico.
Carlos Domínguez-ReyesFundación de Cáncer de Mama, FUCAM, Ciudad de México, Mexico.
Felipe Villegas-CarlosFundación de Cáncer de Mama, FUCAM, Ciudad de México, Mexico.
Elsa Ochoa-MendozaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico.
Alfredo Hidalgo-MirandaLaboratorio de Genómica del Cáncer, Instituto Nacional de Medicina Genómica, Periferico Sur 4809, Tlalpan, Arenal Tepepan, 14610, Ciudad de México (CDMX), Mexico. ahidalgo@inmegen.gob.mx.ORCID http://orcid.org/0000-0003-2315-3977
National Institute of Genomic Medicine · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer (BRCA) is a serious public health problem, as it is the most frequent malignant tumor in women worldwide. BRCA is a molecularly heterogenic disease, particularly at gene expression (mRNAs) level. Recent evidence shows that coding RNAs represent only 34% of the total transcriptome in a human cell. The rest of the 66% of RNAs are non-coding, so we might be missing relevant biological, clinical or regulatory information. In this report, we identified nine novel tumor types from TCGA with FAM83H-AS1 deregulation. We used survival analysis to demonstrate that FAM83H-AS1 expression is a marker for poor survival in IHC-detected ER and PR positive BRCA patients and found a significant correlation between FAM83H-AS1 overexpression and tamoxifen resistance. Estrogen and Progesterone receptor expression levels interact with FAM83H-AS1 to potentiate its effect in OS prediction. FAM83H-AS1 silencing impairs two important breast cancer related pathways: cell migration and cell death. Among the most relevant potential FAM83H-AS1 gene targets, we found p63 and claudin 1 (CLDN1) to be deregulated after FAM83H-AS1 knockdown. Using correlation analysis, we show that FAM83H-AS1 can regulate a plethora of cancer-related genes across multiple tumor types, including BRCA. This evidence suggests that FAM83H-AS1 is a master regulator in different cancer types, and BRCA in particular.

Indexed as

AdultAgedAged, 80 and overBreast NeoplasmsCell MovementClaudin-1Drug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedPrognosisProteinsReceptors, EstrogenReceptors, ProgesteroneSurvival AnalysisClaudin-1CLDN1 protein, humanFAM83H protein, humanProteinsReceptors, EstrogenReceptors, ProgesteroneTamoxifenTP63 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID32839509
PMCPMC7445275
OpenAlexW3081142829

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.