Evidence map›Paper›PMID 36172147›Full record

ArticleFrontiers in oncology2022

FTO promotes liver inflammation by suppressing m6A mRNA methylation of IL-17RA.

Xiaojie Gan, Zhihui Dai, Chunmei Ge, Haozan Yin, Yuefan Wang, Jian Tan, Shuhan Sun, Weiping Zhou, Shengxian Yuan, Fu Yang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 35 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

10 authors at 2 institutions in 1 country.

Xiaojie GanThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Zhihui DaiThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Chunmei GeThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Haozan YinThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Yuefan WangThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Jian TanThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Shuhan SunThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Weiping ZhouThe Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, China.
Shengxian YuanThe Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, China.
Fu YangThe department of Medical Genetics, Naval Medical University, Shanghai, China.
Second Military Medical University · CNEastern Hepatobiliary Surgery Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Previous studies have demonstrated that inflammation-related interleukin-17 (IL-17) signaling plays a pivotal role in the pathogenesis of non-alcoholic steatohepatitis (NASH)- and alcoholic liver disease (ALD)-induced hepatocellular carcinoma (HCC). However, rare efforts have been intended at implementing the analysis of N6-methyladenosine (m6A) mRNA methylation to elucidate the underpinning function of the IL-17 receptor A (IL-17RA) during the inflammation-carcinogenesis transformation of HCC. Methods: We performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) using normal, HCC tumor and paired tumor adjacent tissues from patients to investigate the dynamic changes of m6A mRNA methylation in the process of HCC. Additionally, murine non-alcoholic fatty liver disease (NAFLD) model and murine chronic liver injury model were utilized to investigate the role of IL-17RA regulated by m6A mRNA modulator fat mass and obesity-associated (FTO) in chronic hepatic inflammation. Results: MeRIP-seq revealed the reduction of m6A mRNA methylation of IL-17RA in tumor adjacent tissues with chronic inflammation, suggesting the potential role of IL-17RA in the inflammation-carcinogenesis transformation of HCC. Besides, we demonstrated that FTO, rather than methyltransferase-like 3 (METTL3), methyltransferase-like 14 (METTL14), and alkB homolog 5 (ALKBH5) functions as a main modulator for the decrease of m6A mRNA methylation of IL-17RA Conclusions: Overall, we elaborated the underlying mechanisms of the increase of IL-17RA resulting in chronic inflammation

Indexed as

ftoHCCIL-17RAliver inflammationm6ARNA methylation

Identifiers

PMID36172147
PMCPMC9511030
OpenAlexW4295234378

What Socratic 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 Socratic graph.