Evidence map›Paper›PMID 42637267›Full record

ArticleJournal for immunotherapy of cancer2026

LARS2 reprograms mitochondrial metabolism and epigenetically upregulates MHC-I to boost antitumor immunity in nasopharyngeal carcinoma.

Mei Yang, Yongzhen Mo, Daixi Ren, Shun Liu, Qijia Yan, Lei Shi, Pan Chen, Bo Xiang, Rongfang He, Songqing Fan and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal for immunotherapy of cancer, 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

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

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

16 authors.

Mei YangNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Yongzhen MoKey Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and Xiangya School of Basic Medical Sciences, Central South University, Changsha, Hunan, China.
Daixi RenNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Shun LiuInstitute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Qijia YanDepartment of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
Lei ShiDepartment of Pathology, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Pan ChenNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.ORCID http://orcid.org/0000-0002-0182-2909
Bo XiangNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Rongfang HeInstitute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Songqing FanDepartment of Pathology, the Second Xiangya Hospital, Central South University, Changsha, Hunan, China.
Ming ZhouNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Ming TanNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Guiyuan LiNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China.
Xuyu ZuInstitute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan, China.
Zhaoyang ZengNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China xiongwei@csu.edu.cn zengzhaoyang@csu.edu.cn.
Wei XiongNHC Key Laboratory of Carcinogenesis and Hunan Key Laboratory of Cancer Metabolism, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University, Changsha, Hunan, China xiongwei@csu.edu.cn zengzhaoyang@csu.edu.cn.ORCID http://orcid.org/0000-0003-1635-8173

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNasopharyngeal carcinoma (NPC) is considered a typical "hot" tumor, yet its immune evasion mechanisms remain poorly defined, and immunotherapy efficacy is suboptimal. Attenuation of intrinsic tumor cell immunogenicity to evade T cell recognition and cytotoxicity represents a major route of tumor immune evasion, whose mechanistic basis is largely unelucidated.

methodsMultiplex immunofluorescence and immunohistochemistry were used to assess correlations between mitochondrial leucyl-transfer RNA synthetase 2 (LARS2) expression, CD8

resultsWe demonstrated that LARS2, a gene mapped to the 3p21 chromosomal region, was significantly downregulated in NPC, and its expression is positively correlated with patient prognosis and response to immunotherapy. Through in vitro and in vivo experiments, we demonstrated that restoration of LARS2 expression accelerates the translation of mitochondrial ETC subunits, enhances OXPHOS, and upregulates MHC-I expression via an epigenetic mechanism. These effects work together to enhance tumor antigen presentation and augment CD8

conclusionsThis study uncovers a novel mechanism by which the tumor suppressor LARS2 inhibits immune evasion in NPC through upregulation of MHC-I, and highlights a high-leucine diet as a promising strategy to sensitize tumors to immunotherapy.

Indexed as

Histocompatibility Antigens Class IMitochondriaNasopharyngeal CarcinomaNasopharyngeal NeoplasmsAnimalsCD8-Positive T-LymphocytesCell Line, TumorEpigenesis, GeneticFemaleHumansImmunotherapyMetabolic ReprogrammingMiceMice, NudeUp-RegulationHistocompatibility Antigens Class IHead and Neck CancerImmunotherapyMajor histocompatibility complex - MHC

Identifiers

PMID42637267
PMCPMC13504838

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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.