Evidence map›Paper›PMID 38345740›Full record

ArticleMolecular biology reports2024

Transcriptome-wide profiling identifies colon cancer-associated m6A transcripts and potential RNA methyl modifiers.

Deepa Ramasamy, Megha Thippannah, Hema Raja Pushpam Maharajan, Meenakumari Balaiah, Ramakrishnan Ayloor Seshadri, Ahmad S Kodous, Zdenko Herceg, Anurag Mehta, Arunagiri Kuha Deva Magendhra Rao, Samson Mani

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Article in Molecular biology reports, 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
1.4field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

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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

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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, 6 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Deepa RamasamyDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Megha ThippannahDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Hema Raja Pushpam MaharajanDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Meenakumari BalaiahDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Ramakrishnan Ayloor SeshadriDepartment of Surgical Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Ahmad S KodousDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Zdenko HercegEpigenomics Group, International Agency for Research on Cancer, World Health Organization, Lyon, France.
Anurag MehtaDepartment of Research, Rajiv Gandhi Cancer Institute and Research Centre, Sector 5, Rohini, Delhi, 110085, India.
Arunagiri Kuha Deva Magendhra RaoDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India.
Samson ManiDepartment of Molecular Oncology, Cancer Institute (W.I.A), Chennai, Tamil Nadu, 600036, India. samsonn.m@gmail.com.
Cancer Institute (WIA) · INRajiv Gandhi Cancer Institute and Research Centre · INCentre International de Recherche sur le Cancer · FREgyptian Atomic Energy Authority · EG

Funding

World Health Organization 001
6 · The paper itself

Abstract

backgroundN6-methyladenosine (m6A) is a prevalent and crucial RNA methylation modification that plays a significant role in various biological and pathological processes. The dysregulation of m6A has been linked to the initiation, progression, and metastasis of several cancer types, including colon cancer. The transcriptome of colon cancer indeed provides insight into dysregulated coding and non-coding RNAs, but it does not reveal the mechanisms, such as m6A modifications, that determine post-transcriptional and pre-translational regulations. This study using MeRIP sequencing aims to explain the distribution of m6A modification across altered gene expression and its association with colon cancer. METHODS AND

resultsThe levels of m6A in different colon cancer cell lines were quantified and correlated with the expression of m6A modifiers such as writers, readers, and erasers. Our results showed that global m6A levels in colon cancer were associated with METTL14, YTHDF2, and YTHDC1. We performed Epi-transcriptome profiling of m6A in colon cancer cell lines using Methylated RNA Immunoprecipitation (MeRIP) sequencing. The differential methylation analysis revealed 7312 m6A regions among the colon cancer cell lines. Our findings indicated that the m6A RNA methylation modifications were mainly distributed in the last exonic and 3' untranslated regions. We also discovered that non-coding RNAs such as miRNA, lncRNA, and circRNA carry m6A marks. Gene set enrichment and motif analysis suggested a strong association of m6A with post-transcriptional events, particularly splicing control. Overall, our study sheds light on the potential role of m6A in colon cancer and highlights the importance of further investigation in this area.

conclusionThis study reports m6A enrichment in the last exonic regions and 3' UTRs of mRNA transcripts in colon cancer. METTL14, YTHDF2, and YTHDC1 were the most significant modifiers in colon cancer cells. The functions of m6A-modified genes were found to be RNA methylation and RNA capping. Overall, the study illustrates the transcriptome-wide distribution of m6A and its eminent role in mRNA splicing and translation control of colon cancer.

Indexed as

Colonic NeoplasmsRNAAdenineGene Expression ProfilingHumansRNA, MessengerTranscriptome6-methyladenineAdenineRNARNA, MessengerColon cancerMETTL14N6-methyladenosine or m6ARNA methylationYTHDC1YTHDF2

Identifiers

PMID38345740
OpenAlexW4391746495

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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.