Evidence map›Paper›PMID 42004224›Full record

ArticleGenes & diseases2026

PDK1 elevation was induced by epigenetic modifications of KDM3A and METTL16 to mediate TKI resistance and cancer development.

Zhihao Zhou, Ruike Zhang, Zhaoyang Zhang, Liyuan Zhang, Wei Wang, Wenjing Liu, Chunyang Zhang, Gen Lin, Weimiao Yu, Bo Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Zhihao ZhouTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Ruike ZhangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Zhaoyang ZhangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Liyuan ZhangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Wei WangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Wenjing LiuThe Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, Henan 450000, China.
Chunyang ZhangSchool of Chemistry and Chemical Engineering, State Key Laboratory of Digital Medical Engineering, Southeast University, Nanjing, Jiangsu 211189, China.
Gen LinCancer Center, Beijing Chest Hospital, Capital Medical University & Beijing Tuberculosis and Thoracic Tumor Research Institute, Beijing 101149, China.
Weimiao YuBioinformatics Institute, A∗STAR 138671, Singapore.
Bo XuChongqing Key Laboratory of Intelligent Oncology for Breast Cancer, Intelligent Oncology Innovation Center Designated by the Ministry of Education, Chongqing University Cancer Hospital and Chongqing University School of Medicine, Chongqing 400030, China.
Lin WangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.
Bing-Hua JiangTianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan 450000, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung cancer is the leading cause of cancer-related death and has the second-highest incidence worldwide. For patients with advanced EGFR-mutated non-small cell lung cancer, EGFR tyrosine kinase inhibitors (EGFR-TKIs) are the preferred treatment option; however, acquired resistance to TKIs is inevitable. Gefitinib and osimertinib, the first-generation and third-generation EGFR-TKI, have shown promising results in patients with EGFR-mutated lung cancer in clinical treatment. Here, we identified that pyruvate dehydrogenase kinase 1 (PDK1) was up-regulated in gefitinib- and osimertinib-resistant cell lines, and PDK1 knockdown rendered cells more sensitive to TKI treatment. PDK1 expression levels were significantly increased in lung, colon, liver, and breast cancer tissues compared with those in normal tissues. Histone demethylase KDM3A was also induced in TKI-resistant cell lines, and demethylated histone H3 lysine 9 to facilitate PDK1 expression to regulate TKI resistance. Further study demonstrated that METTL16 promoted the m

Indexed as

KDM3AMETTL16PDK1Prognostic biomarkersTKI resistanceTumorigenesis

Identifiers

PMID42004224
PMCPMC13091346

What Socratic 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 Socratic graph.