Evidence map›Paper›PMID 35354789›Full record

ArticleCell death discovery2022

METTL14 promotes prostate tumorigenesis by inhibiting THBS1 via an m6A-YTHDF2-dependent mechanism.

Yongjie Wang, Junfei Chen, Wei-Qiang Gao, Ru Yang

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  8. The emerging role of mFrontiers in immunology · 2026
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  9. mExperimental & molecular medicine · 2025
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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

4 authors at 1 institution in 1 country.

Yongjie Wang *State Key Laboratory of Oncogenes and Related Genes, Renji-MedX Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 200127, Shanghai, China.ORCID http://orcid.org/0000-0003-4870-2805
Junfei Chen *State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 200032, Shanghai, China.ORCID http://orcid.org/0000-0001-9036-1106
Wei-Qiang GaoState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 200127, Shanghai, China. gao.weiqiang@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-1989-4927
Ru YangState Key Laboratory of Oncogenes and Related Genes, Renji-MedX Clinical Stem Cell Research Center, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, 200127, Shanghai, China. yangruchina@qq.com.ORCID http://orcid.org/0000-0002-6532-7173
Shanghai Jiao Tong University · CN

Funding

Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2017YFA0102900National Natural Science Foundation of China (National Science Foundation of China) 81630073National Natural Science Foundation of China (National Science Foundation of China) 81672485National Natural Science Foundation of China (National Science Foundation of China) 81872406National Natural Science Foundation of China (National Science Foundation of China) 81972343National Natural Science Foundation of China (National Science Foundation of China) 82173356Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) 20JC1417600
6 · The paper itself

Abstract

N6-methyladenine (m6A) is the most predominant RNA modification, which has been shown to be related to many types of cancers. However, understanding of its role in prostate cancer (PCa) is largely unknown. Here, we report an upregulation of METTL14 that was correlated with poor prognosis in PCa patients. Functionally, knocking down METTL14 inhibited tumor proliferation both in vitro and in vivo. Mechanically, RNA-seq and MeRIP-seq analyses identified THBS1 as the downstream target of METTL14 in PCa. METTL14 downregulated THBS1 expression in an m6A-dependent manner, which resulted in the recruitment of YTHDF2 to recognize and degrade Thrombospondin 1 (THBS1) mRNA. Thus, our findings revealed that METTL14 acted as an oncogene by inhibiting THBS1 expression via an m6A-YTHDF2-dependent manner. METTL14 could be a potential prognosis marker and a therapeutic target.

Identifiers

PMID35354789
PMCPMC8967870
OpenAlexW4220797617

What OpenQuestion holds

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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.