Evidence map›Paper›PMID 38287022›Full record

ArticleCell death & disease2024

CYLD induces high oxidative stress and DNA damage through class I HDACs to promote radiosensitivity in nasopharyngeal carcinoma.

Yueshuo Li, Chenxing Yang, Longlong Xie, Feng Shi, Min Tang, Xiangjian Luo, Na Liu, Xudong Hu, Yongwei Zhu, Ann M Bode and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. The CYLD-PARP1 feedback loop regulates DNA damage repair and chemosensitivity in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. HDAC6-mediated deacetylation of FLOT2 maintains stability and tumorigenic function of FLOT2 in nasopharyngeal carcinoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024
    Article
  13. 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

15 authors at 3 institutions in 4 countries.

Yueshuo LiKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Chenxing YangKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Longlong XieChildren's Hospital, Xiangya School of Medicine, Central South University, Changsha, Hunan, 410008, China.
Feng ShiKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Min TangKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Xiangjian LuoKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Na LiuKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Xudong HuKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China.
Yongwei ZhuDepartment of Neurosurgery, National Clinical Research Center for Geriatric Disorders/ Xiangya Hospital, Central South University, Changsha, 410078, China.
Ann M BodeThe Hormel Institute, University of Minnesota, Austin, MN, 55912, USA.
Qiang GaoKey Laboratory for Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Zhongshan Hospital, Shanghai Medical School, Fudan University, Shanghai, 200000, China.ORCID 0000-0002-6695-9906
Jian ZhouKey Laboratory for Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Zhongshan Hospital, Shanghai Medical School, Fudan University, Shanghai, 200000, China.ORCID 0000-0002-2118-1117
Jia FanKey Laboratory for Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Zhongshan Hospital, Shanghai Medical School, Fudan University, Shanghai, 200000, China.ORCID 0000-0001-5158-629X
Xuejun LiKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China. lxjneuro@csu.edu.cn.
Ya CaoKey Laboratory of Carcinogenesis and Cancer Invasion, Chinese Ministry of Education, Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha, 410078, China. ycao98@vip.sina.com.ORCID 0000-0002-3558-3336
Central South University · CNFudan University · CNUniversity of Minnesota · US

Funding

Central South University (Central South University in Hunan) 2022ZZTS0873China Postdoctoral Science Foundation 2022M710170National Natural Science Foundation of China (National Science Foundation of China) 81874172National Natural Science Foundation of China (National Science Foundation of China) 82073030National Natural Science Foundation of China (National Science Foundation of China) 82103019National Natural Science Foundation of China (National Science Foundation of China) 82270825National Natural Science Foundation of China (National Science Foundation of China) 82303137Natural Science Foundation of Hunan Province (Hunan Provincial Natural Science Foundation) 2022JJ20083
6 · The paper itself

Abstract

Abnormal expression of Cylindromatosis (CYLD), a tumor suppressor molecule, plays an important role in tumor development and treatment. In this work, we found that CYLD binds to class I histone deacetylases (HDAC1 and HDAC2) through its N-terminal domain and inhibits HDAC1 activity. RNA sequencing showed that CYLD-HDAC axis regulates cellular antioxidant response via Nrf2 and its target genes. Then we revealed a mechanism that class I HDACs mediate redox abnormalities in CYLD low-expressing tumors. HDACs are central players in the DNA damage signaling. We further confirmed that CYLD regulates radiation-induced DNA damage and repair response through inhibiting class I HDACs. Furthermore, CYLD mediates nasopharyngeal carcinoma cell radiosensitivity through class I HDACs. Thus, we identified the function of the CYLD-HDAC axis in radiotherapy and blocking HDACs by Chidamide can increase the sensitivity of cancer cells and tumors to radiation therapy both in vitro and in vivo. In addition, ChIP and luciferase reporter assays revealed that CYLD could be transcriptionally regulated by zinc finger protein 202 (ZNF202). Our findings offer novel insight into the function of CYLD in tumor and uncover important roles for CYLD-HDAC axis in radiosensitivity, which provide new molecular target and therapeutic strategy for tumor radiotherapy.

Indexed as

Histone Deacetylase InhibitorsNasopharyngeal NeoplasmsDeubiquitinating Enzyme CYLDHistone DeacetylasesHumansNasopharyngeal CarcinomaOxidative StressRepressor ProteinsCYLD protein, humanDeubiquitinating Enzyme CYLDHistone Deacetylase InhibitorsHistone DeacetylasesRepressor ProteinsZNF202 protein, human

Identifiers

PMID38287022
PMCPMC10824711
OpenAlexW4391317680

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.