Evidence map›Paper›PMID 39192337›Full record

ArticleCell communication and signaling : CCS2024

Involvement of HDAC2-mediated kcnq2/kcnq3 genes transcription repression activated by EREG/EGFR-ERK-Runx1 signaling in bone cancer pain.

Zi-Xian Zhang, Yue Tian, Song Li, Hong-Bo Jing, Jie Cai, Min Li, Guo-Gang Xing

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Shaping the Action Potential in Dorsal Root and Trigeminal Ganglia Neurons: Relevance to Pain Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Review
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

7 authors.

Zi-Xian Zhang *Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China.
Yue Tian *Department of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China.
Song LiDepartment of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China.
Hong-Bo JingDepartment of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China.
Jie CaiDepartment of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China.
Min LiDepartment of Anesthesiology, Peking University Third Hospital, Beijing, 100191, China. liminanesth@bjmu.edu.cn.
Guo-Gang XingDepartment of Neurobiology, School of Basic Medical Sciences, Peking University Health Science Center and Neuroscience Research Institute, Peking University, Beijing, China. ggxing@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone cancer pain (BCP) represents a prevalent symptom among cancer patients with bone metastases, yet its underlying mechanisms remain elusive. This study investigated the transcriptional regulation mechanism of Kv7(KCNQ)/M potassium channels in DRG neurons and its involvement in the development of BCP in rats. We show that HDAC2-mediated transcriptional repression of kcnq2/kcnq3 genes, which encode Kv7(KCNQ)/M potassium channels in dorsal root ganglion (DRG), contributes to the sensitization of DRG neurons and the pathogenesis of BCP in rats. Also, HDAC2 requires the formation of a corepressor complex with MeCP2 and Sin3A to execute transcriptional regulation of kcnq2/kcnq3 genes. Moreover, EREG is identified as an upstream signal molecule for HDAC2-mediated kcnq2/kcnq3 genes transcription repression. Activation of EREG/EGFR-ERK-Runx1 signaling, followed by the induction of HDAC2-mediated transcriptional repression of kcnq2/kcnq3 genes in DRG neurons, leads to neuronal hyperexcitability and pain hypersensitivity in tumor-bearing rats. Consequently, the activation of EREG/EGFR-ERK-Runx1 signaling, along with the subsequent transcriptional repression of kcnq2/kcnq3 genes by HDAC2 in DRG neurons, underlies the sensitization of DRG neurons and the pathogenesis of BCP in rats. These findings uncover a potentially targetable mechanism contributing to bone metastasis-associated pain in cancer patients.

Indexed as

Bone NeoplasmsCancer PainErbB ReceptorsGanglia, SpinalHistone Deacetylase 2KCNQ2 Potassium ChannelAnimalsCore Binding Factor Alpha 2 SubunitExtracellular Signal-Regulated MAP KinasesFemaleHumansKCNQ3 Potassium ChannelMAP Kinase Signaling SystemMethyl-CpG-Binding Protein 2RatsRats, Sprague-DawleyCore Binding Factor Alpha 2 SubunitErbB ReceptorsExtracellular Signal-Regulated MAP KinasesHdac2 protein, ratHistone Deacetylase 2KCNQ2 Potassium ChannelKCNQ3 Potassium ChannelKcnq3 protein, ratMecp2 protein, ratMethyl-CpG-Binding Protein 2Repressor ProteinsSIN3A transcription factorSin3 Histone Deacetylase and Corepressor ComplexBone cancer painDorsal root gangliaEpidermal growth factor receptorEpiregulinHistone deacetylase 2Kv7(KCNQ)/M potassium channelsMethyl CpG binding protein 2Transcriptional repression

Identifiers

PMID39192337
PMCPMC11350972

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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.