Evidence map›Paper›PMID 30718500›Full record

ArticleCell death & disease2019

CHD1L contributes to cisplatin resistance by upregulating the ABCB1-NF-κB axis in human non-small-cell lung cancer.

Yang Li, Li-Ru He, Ying Gao, Ning-Ning Zhou, Yurong Liu, Xin-Ke Zhou, Ji-Fang Liu, Xin-Yuan Guan, Ning-Fang Ma, Dan Xie

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. PCK2 Inhibition Reverses Cisplatin Resistance of Non-Small Cell Lung Cancer by Triggering Ferroptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. CHD1L in cancer and beyond: structure, oncogenic functions, and therapeutic potential.Journal of experimental & clinical cancer research : CR · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Versatile function of NF-ĸB in inflammation and cancer.Experimental hematology & oncology · 2024
    Review
  11. Survivin degradation by bergenin overcomes pemetrexed resistance.Cellular oncology (Dordrecht, Netherlands) · 2023
    Article
  12. Article
  13. Article
  14. Activation ofCancers · 2022
    Article
  15. Article
  16. Review
  17. Genome-wide scanning for CHD1L gene in papillary thyroid carcinoma complicated with type 2 diabetes mellitus.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2021
    Article
  18. Article
  19. Article
  20. 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

10 authors at 3 institutions in 1 country.

Yang LiAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Li-Ru HeState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China.
Ying GaoDepartment of Oncology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Ning-Ning ZhouState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China.
Yurong LiuAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China.
Xin-Ke ZhouThe Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Ji-Fang LiuThe Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Xin-Yuan GuanState Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, Guangdong, China.
Ning-Fang MaAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China. nfma@gzhmu.edu.cn.
Dan XieAffiliated Cancer Hospital & Institute of Guangzhou Medical University; Laboratory of Protein Modification and Degradation, State Key Laboratory of Respiratory Disease, Guangzhou Medical University, Guangzhou, Guangdong, 511436, China. xiedan@sysucc.org.cn.
Sun Yat-sen University · CNGuangzhou Medical University · CNSun Yat-sen University Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromodomain helicase/ATPase DNA binding protein 1-like gene (CHD1L) is a recently identified gene associated with malignant tumor progression and patient chemotherapy resistance in human hepatocellular carcinoma (HCC). Previously, we found an association between CHD1L overexpression and poor patient survival in non-small-cell lung cancer (NSCLC). However, little is known about the relationship between CHD1L expression and chemotherapy resistance of NSCLC. By employing immunohistochemistry, we analyzed the expression of CHD1L in NSCLC samples and elucidated the roles and mechanism of CHD1L in NSCLC chemoresistance. We found that the increased expression of CHD1L is positively correlated with a shorter survival time of patients who had received chemotherapy after surgery. We also found that the expression of CHD1L was increased after cisplatin treatment in A549 cells. Conversely, the depletion of CHD1L in cisplatin-resistance cells increased the cell sensitivity to cisplatin, indicating that CHD1L plays a critical role in cisplatin resistance of NSCLC cells. Importantly, we identified the ATP-Binding Cassette Sub-Family B Member (ABCB1) gene as a potential downstream target of CHD1L in NSCLC cells. Knocking down ABCB1 coupled with ectopic expression of CHD1L enhanced the effect of cisplatin on NSCLC cells apoptosis. In addition, overexpressed CHD1L increase the transcription of c-Jun which targeted directly to the promoter of ABCB1. Our data demonstrate that CHD1L could induce cisplatin resistance in NSCLC via c-Jun-ABCB1-NF-κB axis, and may serve as a novel predictive marker and the potential therapeutic target for cisplatin resistance in NSCLC.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsApoptosisATP Binding Cassette Transporter, Subfamily BCarcinoma, Non-Small-Cell LungCisplatinDNA-Binding ProteinsDNA HelicasesDrug Resistance, NeoplasmFemaleGene Expression Regulation, NeoplasticHumansLung NeoplasmsMaleMiceABCB1 protein, humanAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BCHD1L protein, humanCisplatinDNA-Binding ProteinsDNA HelicasesNF-kappa BProto-Oncogene Proteins c-jun

Identifiers

PMID30718500
PMCPMC6362241
OpenAlexW2913372030

What OpenQuestion holds

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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.