Evidence map›Paper›PMID 42469197›Full record

ArticleCell death & disease2026

MAP2K6 reprograms NAD

Ming Wen, Zhuohang Chen, Dongdong Zhan, Mingwei Liu, Shuran Tan, Fang Zhu, Siyu Yang, Jinru Xie, Yu Zhang, Jianjian Li and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Ming WenDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China.
Zhuohang ChenDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China.
Dongdong ZhanState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, China.
Mingwei LiuState Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics, Beijing, China.ORCID http://orcid.org/0000-0001-7061-847X
Shuran TanNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Fang ZhuNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Siyu YangNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Jinru XieDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China.
Yu ZhangNational Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha, China.
Jianjian LiDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China.
Lunquan SunDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China. lunquansun@csu.edu.cn.ORCID http://orcid.org/0000-0002-0558-5250
Rong TanDepartment of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha, China. rongtan@csu.edu.cn.ORCID http://orcid.org/0000-0002-3629-8668

Funding

National Natural Science Foundation of China (National Science Foundation of China) 2025JJ60742National Natural Science Foundation of China (National Science Foundation of China) 81974451
6 · The paper itself

Abstract

PARP inhibitors (PARPi) selectively target cancers with homologous recombination deficiency (HRD), yet emerging evidence suggests that additional determinants beyond BRCA/HRD status modulate PARPi response. Here, by integrating unbiased proteomic profiling with systematic drug-response phenotyping across 11 ovarian cancer cell lines, we identify MAP2K6 as a previously unrecognized regulator of PARP1 activation and an important determinant of PARP inhibitor sensitivity in BRCA-wild-type ovarian cancer. MAP2K6 promotes global PARP1-mediated PARylation and enhances cellular responsiveness to the PARP inhibitor olaparib both in vitro and in vivo. Mechanistically, MAP2K6 can phosphorylate and activate HMGA1, which in turn transcriptionally upregulates NAMPT, resulting in increased intracellular NAD

Indexed as

CytokinesNADNicotinamide PhosphoribosyltransferaseOvarian NeoplasmsPoly(ADP-ribose) Polymerase InhibitorsAnimalsCell Line, TumorFemaleHMGA1a ProteinHumansMicePhthalazinesPiperazinesPoly (ADP-Ribose) Polymerase-1CytokinesHMGA1a ProteinHMGA1 protein, humanNADNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanolaparibPARP1 protein, humanPhthalazinesPiperazinesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID42469197
PMCPMC13658224

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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.