Evidence map›Paper›PMID 40279682›Full record

ArticleNeoplasia (New York, N.Y.)2025

DNA-methylation eraser TET2 activates WTIP expression to suppress an AKT-dependent chemoresistance of gastric cancer.

Yan Guo, Hongyang Yu, Jinyang Li, Kewei Liu, Mengyi Han, Yuxin Tang, Li Su, Xianfeng Li, Haixia Wu, Dongfeng Chen

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neoplasia (New York, N.Y.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Yan GuoDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Hongyang YuDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Jinyang LiDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Kewei LiuDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Mengyi HanDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Yuxin TangDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Li SuDepartment of Oncology and Hematology, Chongqing Hospital of Traditional Chinese Medicine, Chongqing, China.
Xianfeng LiDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China.
Haixia WuSchool of Medical Technology, Chongqing Medical and Pharmaceutical College, Chongqing, China. Electronic address: wuhaihai90@163.com.
Dongfeng ChenDepartment of Gastroenterology, Chongqing Key Laboratory of Digestive Malignancies, Daping Hospital, Army Medical University (Third Military Medical University), Chongqing 400042, China. Electronic address: chendf@tmmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemoresistance is one of the major causes of the failure in gastric cancer (GC) treatment and leads to poor clinical outcomes. Ten-eleven translocation (TET) 2 expression and activity are frequently reduced in solid tumors. However, whether TET2 participants in GC chemoresistance remains poorly understood. In this study, we demonstrated that the TET2 acts as a novel suppressor of GC chemoresistance. TET2 and transcription factor PATZ1 work together to promote the expression of WTIP. WTIP interacts with PP2A to inhibit the T308 phosphorylation and kinase activity of AKT, thereby suppressing stemness and chemoresistance of GC. Thus, the novel TET2-WTIP transcriptional axis, which is frequently silenced, suppresses an AKT-dependent chemoresistance of GC. TET2, combined with WTIP and AKT-pT308, can synergistically serve as a biomarker for predicting chemotherapy response in GC patients. Furthermore, we highlight that combining AKT inhibitor with chemotherapy is a promising therapeutic strategy for TET2-silenced GCs with chemoresistance in clinic.

Indexed as

Carrier ProteinsDNA-Binding ProteinsDNA MethylationDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticProto-Oncogene ProteinsProto-Oncogene Proteins c-aktStomach NeoplasmsAnimalsCell Line, TumorDioxygenasesHumansMiceCarrier ProteinsDioxygenasesDNA-Binding ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-aktTET2 protein, humanChemoresistanceGastric cancerStemnessTET2

Identifiers

PMID40279682
PMCPMC12434994

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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.