Evidence map›Paper›PMID 24525731›Full record

ArticleCell death & disease2014

TXNL1-XRCC1 pathway regulates cisplatin-induced cell death and contributes to resistance in human gastric cancer.

W Xu, S Wang, Q Chen, Y Zhang, P Ni, X Wu, J Zhang, F Qiang, A Li, O D Røe and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  7. Article
  8. Article
  9. Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025
    Review
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  20. Activated STAT3 Is a Novel Regulator of theInternational journal of molecular sciences · 2021
    Article
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

14 authors at 6 institutions in 3 countries.

W Xu1] Department of Molecular Cell Biology and Toxicology, Key Laboratory of Modern Toxicology (NJMU), Ministry of Education, Nanjing, People's Republic of China [2] Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing, People's Republic of China [3] School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
S Wang1] Department of Molecular Cell Biology and Toxicology, Key Laboratory of Modern Toxicology (NJMU), Ministry of Education, Nanjing, People's Republic of China [2] Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing, People's Republic of China [3] School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
Q Chen1] Department of Molecular Cell Biology and Toxicology, Key Laboratory of Modern Toxicology (NJMU), Ministry of Education, Nanjing, People's Republic of China [2] Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing, People's Republic of China [3] School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
Y ZhangDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, People's Republic of China.
P NiDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, People's Republic of China.
X WuDepartment of Oncology, Nantong Cancer Hospital, Jiangsu Province, People's Republic of China.
J ZhangDepartment of Oncology, Nantong Cancer Hospital, Jiangsu Province, People's Republic of China.
F QiangDepartment of Oncology, Nantong Cancer Hospital, Jiangsu Province, People's Republic of China.
A Li1] Department of Molecular Cell Biology and Toxicology, Key Laboratory of Modern Toxicology (NJMU), Ministry of Education, Nanjing, People's Republic of China [2] Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing, People's Republic of China [3] School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
O D Røe1] Department of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway [2] Cancer Clinic, LevangerHospital, Nord-Trøndelag Health Trust, Levanger, Norway.
S XuDepartment of Cell Biology, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, People's Republic of China.
M WangDepartment of Biomedical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX, USA.
R ZhangDepartment of Pharmaceutical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX, USA.
J Zhou1] Department of Molecular Cell Biology and Toxicology, Key Laboratory of Modern Toxicology (NJMU), Ministry of Education, Nanjing, People's Republic of China [2] Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing, People's Republic of China [3] School of Public Health, Nanjing Medical University, Nanjing, People's Republic of China.
Nanjing Medical University · CNMinistry of Education of the People's Republic of China · CNNantong Tumor Hospital · CNTexas Tech University Health Sciences Center · USJiangsu Cancer Hospital · CNNorwegian University of Science and Technology · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cisplatin is a cytotoxic platinum compound that triggers DNA crosslinking induced cell death, and is one of the reference drugs used in the treatment of several types of human cancers including gastric cancer. However, intrinsic or acquired drug resistance to cisplatin is very common, and leading to treatment failure. We have recently shown that reduced expression of base excision repair protein XRCC1 (X-ray repair cross complementing group1) in gastric cancerous tissues correlates with a significant survival benefit from adjuvant first-line platinum-based chemotherapy. In this study, we demonstrated the role of XRCC1 in repair of cisplatin-induced DNA lesions and acquired cisplatin resistance in gastric cancer by using cisplatin-sensitive gastric cancer cell lines BGC823 and the cisplatin-resistant gastric cancer cell lines BGC823/cis-diamminedichloridoplatinum(II) (DDP). Our results indicated that the protein expression of XRCC1 was significantly increased in cisplatin-resistant cells and independently contributed to cisplatin resistance. Irinotecan, another chemotherapeutic agent to induce DNA damaging used to treat patients with advanced gastric cancer that progressed on cisplatin, was found to inhibit the expression of XRCC1 effectively, and leading to an increase in the sensitivity of resistant cells to cisplatin. Our proteomic studies further identified a cofactor of 26S proteasome, the thioredoxin-like protein 1 (TXNL1) that downregulated XRCC1 in BGC823/DDP cells via the ubiquitin-proteasome pathway. In conclusion, the TXNL1-XRCC1 is a novel regulatory pathway that has an independent role in cisplatin resistance, indicating a putative drug target for reversing cisplatin resistance in gastric cancer.

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisCamptothecinCell Line, TumorCisplatinDNA-Binding ProteinsDNA DamageDNA RepairDose-Response Relationship, DrugGene Expression Regulation, NeoplasticHumansIrinotecanProteasome Endopeptidase ComplexRNA InterferenceSignal TransductionAntineoplastic AgentsCamptothecinCisplatinDNA-Binding ProteinsIrinotecanProteasome Endopeptidase ComplexThioredoxinsTXNL1 protein, humanX-ray Repair Cross Complementing Protein 1XRCC1 protein, human

Identifiers

PMID24525731
PMCPMC3944244
OpenAlexW2000377372

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.