Evidence map›Paper›PMID 30092824›Full record

ArticleClinical epigenetics2018

Histone demethylase JARID1B/KDM5B promotes aggressiveness of non-small cell lung cancer and serves as a good prognostic predictor.

Kuang-Tai Kuo, Wen-Chien Huang, Oluwaseun Adebayo Bamodu, Wei-Hwa Lee, Chun-Hua Wang, M Hsiao, Liang-Shun Wang, Chi-Tai Yeh

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
3.6field-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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

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  17. Targeting epigenetic regulators to overcome drug resistance in cancers.Signal transduction and targeted therapy · 2023
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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 5 institutions in 1 country.

Kuang-Tai KuoDivision of Thoracic Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Wen-Chien HuangDivision of Thoracic Surgery, Department of Surgery, MacKay Memorial Hospital, Taipei, Taiwan.
Oluwaseun Adebayo BamoduDepartment of Medical Research and Education, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Wei-Hwa LeeDepartment of Pathology, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
Chun-Hua WangDepartment of Dermatology, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City, Taiwan.
M HsiaoGenomics Research Center, Academia Sinica, Taipei, Taiwan.
Liang-Shun WangDivision of Thoracic Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan. wangls72269@yahoo.com.tw.
Chi-Tai YehDepartment of Medical Research and Education, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan. ctyeh@s.tmu.edu.tw.
Taipei Medical University-Shuang Ho Hospital · TWGenomics Research Center, Academia Sinica · TWMackay Memorial Hospital · TWTaipei Medical University · TWTzu Chi University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung cancer is the leading cause of cancer death worldwide. Recently, epigenetic dysregulation has been known to promote tumor progression and therefore may be a therapeutic target for anticancer therapy. JARID1B, a member of histone demethylases, has been found to be related to tumorigenesis in certain kinds of cancers. However, its biological roles in non-small cell lung cancer (NSCLC) remain largely unclear.

methodsWe firstly examined the expression of JARID1B in surgical specimens and six NSCLC cell lines. Then, we evaluated the relationship between JARID1B expression and clinicopathologic parameters in 72 NSCLC patients, thereby established its prognostic importance. We subsequently studied the functional roles of JARID1B in tumorigenesis to verify its clinicopathologic significance.

resultsOur results showed that JARID1B was overexpressed in NSCLC cells and JARID1B overexpression was associated with tumor size, lymph node metastasis, advanced stages, and poor overall survival in NSCLC patients. JARID1B overexpression resulted in increased cell proliferation and formation of tumorspheres and correlated positively with the expression of cancer stem cells (CSCs) and epithelial-mesenchymal transition (EMT) markers, while the c-Met signaling pathway was actively involved. It also correlated with the strength of resistance to cisplatin and doxorubicin. On the contrary, downregulation of JARID1B expression by applying shRNA or JARID1B inhibitor PBIT reversed these phenomena.

conclusionsJARID1B worsens prognosis of NSCLC patients by promotion of tumor aggressiveness through multiple biological facets which were associated with activation of the c-Met signaling, and can be a novel prognostic biomarker and therapeutic target for NSCLC.

Indexed as

Drug Resistance, NeoplasmUp-RegulationCarcinoma, Non-Small-Cell LungCell Line, TumorCell MovementCell ProliferationCisplatinDNA MethylationDoxorubicinEpigenesis, GeneticEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansJumonji Domain-Containing Histone DemethylasesLung NeoplasmsLymphatic MetastasisCisplatinDoxorubicinJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanNuclear ProteinsRepressor ProteinsCancer stem cellsc-MetJARID1BLung cancerPrognosis

Identifiers

PMID30092824
PMCPMC6085612
OpenAlexW2886320087

What OpenQuestion holds

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Read underepoch 390

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.