Evidence map›Paper›PMID 35776197›Full record

ArticleJournal of cancer research and clinical oncology2022

T helper cell-mediated epitranscriptomic regulation via m6A RNA methylation bridges link between coronary artery disease and invasive ductal carcinoma.

Sudeshna Rakshit, Jithin S Sunny, Melvin George, Luke Elizabeth Hanna, K V Leela, Koustav Sarkar

Open access · greenAbstract read
In one paragraph

Article in Journal of cancer research and clinical oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
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

9 citing papers in PubMed, 31 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

6 authors at 2 institutions in 1 country.

Sudeshna RakshitDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, 603203, India.ORCID http://orcid.org/0000-0002-7496-3155
Jithin S SunnyDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, 603203, India.ORCID http://orcid.org/0000-0002-8811-3565
Melvin GeorgeDepartment of Clinical Pharmacology, SRM Medical College Hospital and Research Center, Kattankulathur, Tamil Nadu, 603203, India.ORCID http://orcid.org/0000-0002-8198-6144
Luke Elizabeth HannaDepartment of HIV/AIDS, National Institute for Research in Tuberculosis, Chetpet, Tamil Nadu, 600031, India.ORCID http://orcid.org/0000-0002-6299-8211
K V LeelaDepartment of Microbiology, SRM Medical College Hospital and Research Center, Kattankulathur, Tamil Nadu, 603203, India.
Koustav SarkarDepartment of Biotechnology, SRM Institute of Science and Technology, Kattankulathur, Tamil Nadu, 603203, India. koustavsarkar@gmail.com.ORCID http://orcid.org/0000-0002-0696-6688
SRM Institute of Science and Technology · INNational Institute of Research in Tuberculosis · IN

Funding

Science and Engineering Research Board ECR/2016/000965
6 · The paper itself

Abstract

purposeInvasive ductal carcinoma (IDC) and coronary artery disease (CAD), remains the greatest cause of death annually in women, driven by complex signalling pathways and shared several predisposing risk factors together. Therefore, it is important to find out the common epigenetic modifications which are responsible for possible disease progression from CAD to IDC.

methodsCD4+T cell isolation by MACS, RT2 profiler PCR array, Gene ontology study, m6A RNA methylation, ChIP-qPCR, Q-PCR, CRISPR/Cas9-mediated knockout/overexpression, Lactate dehydrogenase release assay, RDIP-qPCR.

resultsWe have identified several epigenetic regulators (e.g., VEGFA, AIMP1, etc.) which are mainly involved in inflammatory pathways in both the diseased conditions. Epitranscriptomic alterations such as m6A RNA methylation found abnormal in CD4+T helper cells in both IDC as well as CAD. CRISPR-Cas9 mediated knockout/overexpression of specific gene (BRCA1) are promising therapeutic approaches in diseased conditions by regulating m6A RNA methylation and also tumor suppressor gene P53. It also affected the R-loop formation which is vulnerable to DNA damage and BRCA1 can also induce CTL mediated cytotoxicity in breast cancer cells.

conclusionsTherefore, by understanding the modifications of epigenetic mechanisms, their alterations and interactions will aid in the development of newer therapeutic approaches to stop the possible spread from one disease to another.

Indexed as

Carcinoma, DuctalCoronary Artery DiseaseFemaleHumansLactate DehydrogenasesMethylationRNAT-Lymphocytes, Helper-InducerTumor Suppressor Protein p53Lactate DehydrogenasesRNATumor Suppressor Protein p53AIMP1BRCA1InflammationP53R-loopVEGFA

Identifiers

PMID35776197
PMCPMC11800896
OpenAlexW4283763046

What OpenQuestion holds

Textmetadata
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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.