Evidence map›Paper›PMID 41904143›Full record

ArticleNature communications2026

NEK8 kinase-mediated lactate increase impairs antitumor immunity decreasing radiotherapy sensitivity in colorectal cancer.

Mingzhou Li, Yunfei Ni, Jieqiong Wu, Xin Zou, Yining Chen, Junfeng Qiu, Yifang Li, Huayu Cai, Li Wang, Feifei Wang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

16 authors.

Mingzhou Li *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0007-4556-9822
Yunfei Ni *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Jieqiong Wu *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Xin Zou *Department of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0003-1199-5018
Yining ChenDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0007-5197-4074
Junfeng QiuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0000-7491-9720
Yifang LiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0006-8349-211X
Huayu CaiDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0004-7101-8176
Li WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0005-5501-0438
Feifei WangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0000-0002-5962-3136
Hongxia ZhangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0004-5382-115X
Fangyi HanDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0000-6257-3080
Jinghao HuangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0004-7370-6212
Zilong ChenDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.
Bingyu XuDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China.ORCID http://orcid.org/0009-0006-0192-6034
Li LiangDepartment of Pathology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China. lli@smu.edu.cn.ORCID http://orcid.org/0000-0001-5302-2754

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Radiotherapy effectively treats colorectal cancer (CRC), but local recurrence remains common and abscopal effects-regression of tumors distant from irradiated sites-are rarely observed even with immune checkpoint inhibitors. Here we show that the protein kinase NEK8, highly expressed in CRC, promotes radioresistance by suppressing anti-tumor immunity. In radiation-resistant tumors, NEK8 phosphorylates lactate dehydrogenase A (LDHA), driving lactate overproduction. This metabolite promotes histone modifications that silence antigen presentation machinery, while extracellular lactate directly impairs CD8

Indexed as

Colorectal NeoplasmsLactic AcidNIMA-Related KinasesRadiation ToleranceAnimalsCD8-Positive T-LymphocytesCell Line, TumorHumansLactate Dehydrogenase 5MicePhosphorylationTumor MicroenvironmentLactate Dehydrogenase 5Lactic AcidNIMA-Related Kinases

Identifiers

PMID41904143
PMCPMC13195097

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.