Evidence map›Paper›PMID 39725712›Full record

ArticleOncogene2025

Mevalonate kinase inhibits anti-tumor immunity by impairing the tumor cell-intrinsic interferon response in microsatellite instability colorectal cancer.

Yuanyu Liao, Rui Yang, Bojun Wang, Yuli Ruan, Luying Cui, Jiani Yang, Xuefan Yu, Shuling Han, Yuanfei Yao, Xindi Luan and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Review
  2. Article
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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

15 authors.

Yuanyu Liao *Department of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.ORCID http://orcid.org/0000-0003-1139-1361
Rui Yang *Department of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Bojun Wang *Department of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yuli RuanDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Luying CuiDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Jiani YangDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Xuefan YuDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Shuling HanDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yuanfei YaoDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Xindi LuanDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Yingjue LiDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Mengde ShiDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Shuijie LiState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Department of Biopharmaceutical Sciences, College of Pharmacy, Harbin Medical University, Harbin, China. shuijie.li@hrbmu.edu.cn.
Chao LiuDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China. liuchao@hrbmu.edu.cn.
Yanqiao ZhangDepartment of Gastrointestinal Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China. yanqiaozhang@ems.hrbmu.edu.cn.ORCID http://orcid.org/0000-0002-6206-8364

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82102858National Natural Science Foundation of China (National Science Foundation of China) 82173233National Natural Science Foundation of China (National Science Foundation of China) 82373372National Natural Science Foundation of China (National Science Foundation of China) U22A20330
6 · The paper itself

Abstract

Insufficient tumor cell-intrinsic interferon response represents a major obstacle in immune checkpoint blockade (ICB) therapy, particularly in anti-PD-1 treatment. Although cholesterol metabolism has been demonstrated to be a critical regulator of anti-tumor immune responses, whether cholesterol influences tumor cell-intrinsic interferon response in microsatellite instability (MSI) colorectal cancer (CRC) remains unknown. Through comprehensive siRNA library screening and Gene Set Enrichment Analysis (GSEA), we identified mevalonate kinase (MVK) as a crucial negative regulator of tumor cell-intrinsic interferon response in MSI CRC cells. Genetic ablation of MVK resulted in significant upregulation of Th1 type chemokines (CXCL9 and CXCL10) and enhanced CD8

Indexed as

Colorectal NeoplasmsInterferonsMicrosatellite InstabilityPhosphotransferases (Alcohol Group Acceptor)AnimalsCell Line, TumorDisease ProgressionFemaleHumansImmunotherapyMiceMicrosatellite RepeatsPhosphorylationSignal TransductionSTAT1 Transcription FactorTh1 CellsInterferonsmevalonate kinasePhosphotransferases (Alcohol Group Acceptor)STAT1 protein, humanSTAT1 Transcription Factor

Identifiers

What OpenQuestion holds

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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.