Evidence map›Paper›PMID 40615689›Full record

ArticleOncogene2025

HDAC1/2-mediated deacetylation of KLF9 promotes the malignant progression of nasopharyngeal carcinoma via CDH17.

Kun Zhang, Xingzhi Peng, Peijun Zhou, Xuanxuan Li, Liangfang Shen, Lifang Yang, Qin Zhou

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Kun ZhangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0002-1320-9095
Xingzhi PengDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.ORCID http://orcid.org/0000-0002-1516-0731
Peijun ZhouDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Xuanxuan LiDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Liangfang ShenDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Lifang YangDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. yanglifang@csu.edu.cn.ORCID http://orcid.org/0000-0002-3012-8350
Qin ZhouDepartment of Oncology, Key Laboratory of Carcinogenesis and Cancer Invasion of Ministry of Education, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China. zhouqin5796@csu.edu.cn.ORCID http://orcid.org/0000-0002-5003-161X

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82372683Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation) 2022JJ30059Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation) 2024JJ5616
6 · The paper itself

Abstract

Protein acetylation modifications play an important role in the malignant progression and metastasis of tumors. The transcription factor KLF9 primarily functions as a transcriptional suppressor exerting anticancer effects in some tumors. However, the expression regulation of KLF9 and its role in nasopharyngeal carcinoma (NPC) are not well understood. In the present study, we found that KLF9 exhibited deacetylation and low expression in NPC, and its overexpression inhibited the proliferation and metastasis of NPC. Mechanistically, the high expression of HDAC1/2 in tumor cells mediated the deacetylation of KLF9 at lysine 237/238, further inhibiting the K63 ubiquitination induced by the E3 ubiquitin ligase SYVN1, thus reducing the protein stability and subsequent transcriptional inhibition function of KLF9. Meanwhile, we found that KLF9 could restrain the transcription and expression of cadherin-17 (CDH17), suppressing the malignant progression and metastasis of NPC. This research expands our comprehension of transcription factor expression regulation from the perspective of protein acetylation and ubiquitination interactions, providing novel molecular markers and therapeutic targets for NPC.

Indexed as

CadherinsHistone Deacetylase 1Histone Deacetylase 2Kruppel-Like Transcription FactorsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsAcetylationAnimalsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceUbiquitinationUbiquitin-Protein LigasesCadherinsHDAC1 protein, humanHDAC2 protein, humanHistone Deacetylase 1Histone Deacetylase 2Kruppel-Like Transcription FactorsUbiquitin-Protein Ligases

Identifiers

PMID40615689

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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.