Evidence map›Paper›PMID 42126535›Full record

ArticleCellular and molecular life sciences : CMLS2026

NAT10-mediated crosstalk between acetylation and PARylation enhances the function of PARP1 promoting primary resistance in esophageal cancer.

Yake Chen, Sizhen Hou, Boyuan Jiang, Yang Yang, Yisi Fan, Xinyue Huang, Fengxiang Liu, Wenjing An, Qiaocen Geng, Jie Yin and 8 more

Abstract read
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In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

18 authors.

Yake Chen *Xinxiang Medical University, Xinxiang, 453000, China.
Sizhen Hou *Xinxiang Medical University, Xinxiang, 453000, China.
Boyuan JiangXinxiang Medical University, Xinxiang, 453000, China.
Yang YangXinxiang Medical University, Xinxiang, 453000, China.
Yisi FanXinxiang Medical University, Xinxiang, 453000, China.
Xinyue HuangXinxiang Medical University, Xinxiang, 453000, China.
Fengxiang LiuXinxiang Medical University, Xinxiang, 453000, China.
Wenjing AnXinxiang Medical University, Xinxiang, 453000, China.
Qiaocen GengXinxiang Medical University, Xinxiang, 453000, China.
Jie YinXinxiang Medical University, Xinxiang, 453000, China.
Huiqin ZhengXinxiang Medical University, Xinxiang, 453000, China.
Kexin GuoXinxiang Medical University, Xinxiang, 453000, China.
Ting LiXinxiang Medical University, Xinxiang, 453000, China.
Wenwen ZhaoXinxiang Medical University, Xinxiang, 453000, China.
Zhijian DengDepartment of Clinical Pharmacy, the First Affiliated Hospital of Xinxiang Medical University, Xinxiang, 453100, China.
Di HanXinxiang Medical University, Xinxiang, 453000, China. hd@xxmu.edu.cn.
Heng LiYong Loo Lin School of Medicine, National University of Singapore, Singapore, 117456, Singapore. liheng@nus.edu.sg.
Yu SongXinxiang Medical University, Xinxiang, 453000, China. songyulab@xxmu.edu.cn.ORCID http://orcid.org/0000-0002-3803-8464

Funding

Henan Province Key Subjects of Clinical Pharmacy Henan Province Key Subjects of Clinical PharmacyHenan Provincial Science and Technology Fund 232102310442
6 · The paper itself

Abstract

Resistance to platinum-based drugs represents a significant challenge in the clinical treatment of esophageal cancer. Particularly, some esophageal cancer patients exhibit primary resistance to platinum-based drugs. Our study revealed that the level of N-acetyltransferase 10 (NAT10) is inversely correlated with the efficacy of platinum-based drug neoadjuvant therapy. In the presence of oxaliplatin, NAT10 significantly reduced the cytotoxicity of oxaliplatin and enhanced esophageal cancer cells' invasive, migratory, and clonogenic abilities. Mechanistically, oxaliplatin promoted the binding of NAT10 to PARP1. NAT10 acetylated PARP1 at the K97 site, thereby enhancing its stability. Additionally, acetylated PARP1 increased its PARylation modification, promoting the recruitment of downstream DNA repair proteins. In conclusion, NAT10 contributes to primary resistance by regulating the crosstalk of acetylation and PARylation of PARP1 in esophageal cancer.

Indexed as

Drug Resistance, NeoplasmEsophageal NeoplasmsN-Terminal Acetyltransferase EPoly (ADP-Ribose) Polymerase-1AcetylationAntineoplastic AgentsCell Line, TumorCell MovementHumansN-Terminal AcetyltransferasesOxaliplatinAntineoplastic AgentsNAT10 protein, humanN-Terminal Acetyltransferase EN-Terminal AcetyltransferasesOxaliplatinPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1AcetylationEsophageal cancerN-acetyltransferase 10PARylationPrimary resistance

Identifiers

PMID42126535
PMCPMC13337986

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LicenceCC BY-NC-ND
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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.