Evidence map›Paper›PMID 36114757›Full record

ArticleCancer science2022

m6A modification-mediated lncRNA TP53TG1 inhibits gastric cancer progression by regulating CIP2A stability.

Deliang Fang, Xinde Ou, Kaiyu Sun, Xingyu Zhou, Youpei Li, Peng Shi, Zirui Zhao, Yulong He, Jianjun Peng, Jianbo Xu

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed
10.1field-weighted citation impact, top 1% 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

86 citing papers in PubMed, 120 citations in OpenAlex.

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  12. mFrontiers in cell and developmental biology · 2026
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  16. LncRNA-Histone Modification Crosstalk: Orchestrating Cancer Pathobiology.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  17. Article
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26 more citing papers are in PubMed but not listed here.

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.

Deliang FangDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xinde OuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Kaiyu SunDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Xingyu ZhouDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Youpei LiDepartment of Anesthesiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
Peng ShiHuazhong University of Science and Technology Union Shenzhen Hospital, Shenzhen, China.
Zirui ZhaoDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Yulong HeDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Jianjun PengDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Jianbo XuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.ORCID https://orcid.org/0000-0001-9143-168X
Sun Yat-sen University · CNUnion Hospital · CN

Funding

National Natural Science Foundation of China 81672343National Natural Science Foundation of China 81871915Natural Science Foundation of Guangdong, China 2017A030313570Natural Science Foundation of Guangdong, China 2018A030313543Natural Science Foundation of Guangdong, China 2022A1515012140
6 · The paper itself

Abstract

Long noncoding RNAs (lncRNAs) are associated with various types of cancer. However, the precise roles of many lncRNAs in tumor progression remain unclear. In this study, we found that the expression of the lncRNA TP53TG1 was downregulated in gastric cancer (GC) and it functioned as a tumor suppressor. In addition, low TP53TG1 expression was significantly associated with poor survival in patients with GC. TP53TG1 inhibited the proliferation, metastasis, and cell cycle progression of GC cells, while it promoted their apoptosis. m6A modification sites are highly abundant on TP53TG1, and demethylase ALKBH5 reduces TP53TG1 stability and downregulates its expression. TP53TG1 interacts with cancerous inhibitor of protein phosphatase 2A (CIP2A) and triggers its ubiquitination-mediated degradation, resulting in the inhibition of the PI3K/AKT pathway. These results suggest that TP53TG1 plays an important role in inhibiting the progression of GC and provides a crucial target for GC treatment.

Indexed as

RNA, Long NoncodingStomach NeoplasmsAutoantigensCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphatidylinositol 3-KinasesAutoantigensCIP2A protein, humanIntracellular Signaling Peptides and ProteinsMembrane ProteinsPhosphatidylinositol 3-KinasesRNA, Long NoncodingALKBH5CIP2Agastric cancerPI3K/AKTTP53TG1

Identifiers

PMID36114757
PMCPMC9746054
OpenAlexW4296120091

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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.