Evidence map›Paper›PMID 32334542›Full record

ArticleBMC cancer2020

Altered ARID1A expression in colorectal cancer.

Mehran Erfani, Seyed Vahid Hosseini, Maral Mokhtari, Mozhdeh Zamani, Kamran Tahmasebi, Mahvash Alizadeh Naini, Alireza Taghavi, John M Carethers, Minoru Koi, Hassan Brim and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

28 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Molecular medicine reports · 2024
    Article
  11. Therapeutic Role of Synthetic Lethality inJournal of immunotherapy and precision oncology · 2024
    Review
  12. Article
  13. Review
  14. ARID1A in cancer: Friend or foe?Frontiers in oncology · 2023
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Evidence of histone modification affectingGastroenterology and hepatology from bed to bench · 2022
    Article
  20. 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

12 authors at 3 institutions in 2 countries.

Mehran ErfaniAutophagy Research Center and Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran.
Seyed Vahid HosseiniColorectal Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Maral MokhtariDepartment of Pathology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Mozhdeh ZamaniColorectal Research Center, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Kamran TahmasebiDepartment of Pathology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Mahvash Alizadeh NainiDepartment of Internal Medicine, Gastroenterology division, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Alireza TaghaviDepartment of Internal Medicine, Gastroenterology division, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
John M CarethersDepartments of Internal Medicine and Human Genetics, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109-5368, USA.
Minoru KoiDepartments of Internal Medicine and Human Genetics, and Rogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109-5368, USA.
Hassan BrimCancer Center and Department of Medicine, Howard University, College of Medicine, 2041 Georgia Avenue, N.W., Washington, D.C., 20060, USA.
Pooneh MokarramAutophagy Research Center and Department of Biochemistry, Shiraz University of Medical Sciences, Shiraz, Iran. mokaram2@gmail.com.
Hassan AshktorabCancer Center and Department of Medicine, Howard University, College of Medicine, 2041 Georgia Avenue, N.W., Washington, D.C., 20060, USA. hashktorab@howard.edu.ORCID http://orcid.org/0000-0002-4048-4666
Shiraz University of Medical Sciences · IRHoward University · USUniversity of Michigan · US

Funding

Sleep Disorders in Adults with Sickle Cell Disease: Frequency, Associations with Cardiovascular and Pain Indicators, and Responses to TreatmentU54MD007597 · NIMHD · HOWARD UNIVERSITY · PI Tatiana V.D. Sanses · 2019 to 2026
$37.7M
PROTEOMICS CORE FACILITYG12MD007597 · NIMHD · HOWARD UNIVERSITY · PI SOUTHERLAND, WILLIAM M. · 2012 to 2018
$14.8M
(PQ3) Immune Modulation of DNA Mismatch Repair in Colorectal CancerR01CA206010 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CARETHERS, JOHN M · 2016 to 2020
$1.8M
NCI NIH HHS R01 CA206010NIH HHS CA206010NIMHD NIH HHS G12 MD007597NIMHD NIH HHS G12MD007597NIMHD NIH HHS U54 MD007597Shiraz University of Medical Sciences 94-9136
6 · The paper itself

Abstract

backgroundARID1A has been described as a tumor suppressor gene, participating in chromatin re-modeling, epithelial-mesenchymal-transition and many other cellular and molecular processes. It has been cited as a contribute in tumorigenesis. The role of ARID1A in CRC is not yet defined.

aimTo investigate the role of ARID1A methylation and CNV in its expression in CRC cell lines and to examine the relationship between ARID1A status with survival and clinicopathologic characteristics in patients with CRC.

methodsWe used RT-PCR to determine both CNV and expression of ARID1A from six CRC cell lines. We used MSP to evaluate methylation of ARID1A. IHC was used to assess ARID1A protein expression. We also evaluated MSI and EMAST status in 18 paired CRC and adjacent normal tissues. 5AzadC was used to assess effect of DNA demethylation on ARID1A expression. Statistical analysis was performed to establish correlations between ARID1A expression and other parameters.

resultsAmong the 18 CRC tumors studied, 7 (38.8%) and 5 tumors (27.7%) showed no or low ARID1A expression, respectively. We observed no significant difference in ARID1A expression for overall patient survival, and no difference between clinicopathological parameters including MSI and EMAST. However, lymphatic invasion was more pronounced in the low/no ARID1A expression group when compared to moderate and high expression group (33% VS. 16.6% respectively. ARID1A promoter methylation was observed in 4/6 (66%) cell lines and correlated with ARID1A mRNA expression level ranging from very low in SW48, to more pronounced in HCT116 and HT-29/219. Treatment with the methyltransferase inhibitor 5-Azacytidine (5-aza) resulted in a 25.4-fold and 6.1-fold increase in ARID1A mRNA expression in SW48 and SW742 cells, respectively, while there was no change in SW480 and LS180 cells. No ARID1A CNV was observed in the CRC cell lines.

conclusionARID1A expression is downregulated in CRC tissues which correlates with it being a tumor suppressor protein. This finding confirms ARID1A loss of expression in CRC development. Our in-vitro results suggest high methylation status associates with reduced ARID1A expression and contributes to CRC tumorigenesis. However, there was no significant association between ARID1A loss of expression and clinicopathological characteristics. Future in-vivo analysis is warranted to further establish ARID1A role in colorectal neoplastic transformation.

Indexed as

DNA MethylationGene Expression Regulation, NeoplasticPromoter Regions, GeneticAntimetabolites, AntineoplasticAzacitidineBiomarkers, TumorColorectal NeoplasmsDNA-Binding ProteinsFemaleHumansMaleMiddle AgedPrognosisSurvival RateTranscription FactorsTumor Cells, CulturedAntimetabolites, AntineoplasticARID1A protein, humanAzacitidineBiomarkers, TumorDNA-Binding ProteinsTranscription FactorsARID1AColorectal cancerImmunohistochemistryMethylation

Identifiers

PMID32334542
PMCPMC7183124
OpenAlexW3017632813

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.