Evidence map›Paper›PMID 41476293›Full record

ArticleExperimental hematology & oncology2025

The lncRNA PARylator promotes PARP1 activation and resistance to DNA‑damaging therapy in esophageal squamous cell carcinoma.

Teng Fei Qi, Yadong Liu, Jinkun Yang, Yi Meng Yue, Man Man Han, Hongtao Liu, Jing Li, Min Liu, Yuwei Zhang, Jia Hui Kou and 9 more

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Article in Experimental hematology & oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

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1 · What the graph read from it

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2 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

19 authors.

Teng Fei QiTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Yadong LiuTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Jinkun YangTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Yi Meng YueTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Man Man HanTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Hongtao LiuSchool of Life Sciences, Zhengzhou University, Zhengzhou, 450001, China.
Jing LiDepartment of Pharmacology, School of Basic Medicine, Zhengzhou Universaity, Zhengzhou, 450001, Henan, China.
Min LiuHenan Province Hypertension Precision Prevention and Control Engineering Research Center, Henan Provincial People's Hospital, Zhengzhou, 450053, China.
Yuwei ZhangHenan Key Laboratory of Stem Cell Differentiation and Modification, Henan Provincial People's Hospital, Henan University, Zhengzhou, 450003, China.
Jia Hui KouSchool of Basic Medical Science, Shanxi Medical University, Taiyuan, 030000, China.
Wen Jin LiSchool of Basic Medical Science, Shanxi Medical University, Taiyuan, 030000, China.
Xiaoying LiuTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Ting LaNational-Local Joint Engineering Research Center of Biodiagnosis & Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710004, China.
Tao LiuTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Song ChenTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Xu Dong ZhangTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China.
Shundong CangDepartment of Oncology, Henan Provincial International Coalition Laboratory of Oncology Precision Treatment, Henan Provincial Academician Workstation of Non-coding RNA Translational Research, Henan Provincial Peoples Hospital, Zhengzhou University People's Hospital, Henan, 450003, China. cangshundong@163.com.
Liu TengTranslational Research Institute of Henan Provincial People's Hospital, Henan International Joint Laboratory of Non-coding RNA and Metabolism in Cancer, Henan Provincial Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Zhengzhou City Key Laboratory of Long Non-coding RNA and Cancer Metabolism, Academy of Medical Sciences and Tianjian Laboratory of Advanced Biomedical Sciences of Zhengzhou University, Zhengzhou, 450053, China. tengliu2007@126.com.
Tianli FanDepartment of Pharmacology, School of Basic Medicine, Zhengzhou Universaity, Zhengzhou, 450001, Henan, China. fantianlipp@163.com.

Funding

Key Project of Henan Provincial Science and Technology R&D Program Joint Fund 225200810011National Natural Science Foundation of China 82303099
6 · The paper itself

Abstract

backgroundOutcomes for patients with esophageal squamous cell carcinoma (ESCC) remain poor, partly due to treatment resistance, particularly to DNA-damaging therapies. Poly(ADP‑ribose) polymerase 1 (PARP1) plays a critical role in repairing single‑strand DNA breaks (SSBs). Unrepaired SSBs can be converted into double‑strand breaks (DSBs) during DNA replication, potentially leading to cell death. Genomic amplification of the distal portion of chromosome 3q (3q26-q29) is a frequent copy‑number alteration in ESCC, which harbors genes encoding several oncoproteins. However, whether long noncoding RNAs (lncRNAs) from this region contribute to ESCC pathogenesis and treatment resistance remains poorly understood.

methodsIn situ hybridization and qPCR were used to assess RNA expression. Protein PARylation was evaluated by immunoprecipitation followed by Western blotting. Cellular phenotypes were quantified using the cell counting kit-8, Annexin V/Propidium iodide staining, and clonogenic assays. DNA damage was monitored by immunofluorescence staining for phosphorylated histone H2AX (γH2AX) and p53-binding protein 1 (53BP1) and by comet assays. RNA-protein interactions were assessed through RNA pulldown coupled with mass spectrometry and RNA immunoprecipitation. Chromatin fractionation and detergent pre-extraction immunofluorescence were conducted to examine PARP1 chromatin association. ESCC growth and responses to treatments were evaluated using xenograft models.

resultsThe lncRNA LINC00885, hereafter referred to as PARylator, was the most upregulated lncRNA encoded within the 3q26-q29 amplicon in ESCC. PARylator was predominantly nuclear and interacted with PARP1. Knockdown of PARylator increased γH2AX and 53BP1 foci and comet tail moment, triggered apoptosis, reduced clonogenicity, sensitized ESCC cells to cisplatin and ionizing radiation. In vivo, PARylator knockdown impaired tumor growth and increased cisplatin sensitivity in ESCC xenografts. Mechanistically, PARylator promoted PARP1 recruitment to chromatin and catalytic activation, thereby increasing PARP1 auto-PARylation and enhancing the PARylation of X-ray repair cross-complementing 1 (XRCC1). PARylator was further upregulated in response to DNA damage.

conclusionsThe DNA damage-responsive, 3q26-q29 amplicon-encoded lncRNA PARylator promotes PARP1‑mediated PARylation and SSB repair, thereby limiting DSB accumulation and supporting ESCC cell survival and resistance to DNA-damaging therapies. Targeting PARylator, alone or in combination with DNA-damaging agents, may represent a novel avenue for ESCC treatment.

Indexed as

DNA repairEsophageal squamous cell carcinomaLINC00885LncRNAPARP1PARylationPARylator

Identifiers

PMID41476293
PMCPMC12781723

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