Evidence map›Paper›PMID 36195596›Full record

ArticleCell death & disease2022

Upregulation of CRABP2 by TET1-mediated DNA hydroxymethylation attenuates mitochondrial apoptosis and promotes oxaliplatin resistance in gastric cancer.

Xiaolong Tang, Yahang Liang, Guorui Sun, Qingsi He, Zhenyu Hou, Xingzhi Jiang, Peng Gao, Hui Qu

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  4. World journal of gastroenterology · 2026
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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

8 authors at 1 institution in 1 country.

Xiaolong TangDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Yahang LiangDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Guorui SunDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Qingsi HeDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Zhenyu HouDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Xingzhi JiangDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China.
Peng GaoDepartment of Pathology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Hui QuDepartment of General Surgery, Qilu Hospital of Shandong University, Jinan, 250012, China. doctorquhui@email.sdu.edu.cn.ORCID 0000-0003-0061-913X
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxaliplatin is the main chemotherapy drug for gastric cancer (GC), but quite a few patients are resistant to oxaliplatin, which contributes to the poor prognosis of GC patients. There is therefore an urgent need to identify potential targets for reversing chemotherapy resistance in GC patients. In this study, we analyzed the tumor samples of GC patients who received neoadjuvant chemotherapy based on oxaliplatin through quantitative proteomics and identified the potential chemoresistance-related protein cellular retinoic acid binding protein 2 (CRABP2). CRABP2 was significantly upregulated in the tumor tissues of chemoresistant GC patients and was closely related to prognosis. The results of cell function experiments showed that CRABP2 can promote the oxaliplatin resistance of GC cells in vitro. Coimmunoprecipitation and GST pulldown assays showed that CRAPB2 expedited the binding of BAX and PARKIN in GC cells and facilitated the ubiquitination-mediated degradation of BAX. Furthermore, both the in vitro assay and cell-derived xenograft (CDX) in vivo model verified that CRABP2 promoted oxaliplatin resistance by inhibiting BAX-dependent cell apoptosis. Further experiments proved that the abnormally high expression of CRABP2 in oxaliplatin-resistant GC cells was affected by TET1-mediated DNA hydroxymethylation. The patient-derived xenograft (PDX) model suggested that interference with CRABP2 reversed oxaliplatin resistance in GC in vivo. In conclusion, the results of our study show that CRABP2 was a key molecule in oxaliplatin resistance regulation and could be a new target for reversing the chemoresistance of GC.

Indexed as

Stomach NeoplasmsApoptosisbcl-2-Associated X ProteinCell Line, TumorCell ProliferationDNADrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMixed Function OxygenasesOxaliplatinProto-Oncogene ProteinsReceptors, Retinoic AcidUbiquitin-Protein LigasesUp-Regulationbcl-2-Associated X ProteinDNAMixed Function OxygenasesOxaliplatinProto-Oncogene ProteinsReceptors, Retinoic Acidretinoic acid binding protein II, cellularTET1 protein, humanUbiquitin-Protein Ligases

Identifiers

PMID36195596
PMCPMC9532395
OpenAlexW4301399315

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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.