Evidence map›Paper›PMID 42204133›Full record

ArticleSignal transduction and targeted therapy2026

LISS enables immune evasion of colorectal cancers irrespective of MSI status.

Qingyu Lin, Xingwen Wang, Weixu Zhao, Shiying Song, Yi Zhang, Jiangwen Ma, Tianyu Li, Yuhan Wei, Minqiao Lu, Guixue Hou and 8 more

Abstract read
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In one paragraph

Article in Signal transduction and targeted therapy, 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
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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

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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

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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

18 authors.

Qingyu Lin *School of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Xingwen Wang *School of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Weixu ZhaoSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Shiying SongSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Yi ZhangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Jiangwen MaSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Tianyu LiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Yuhan WeiSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Minqiao LuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Guixue HouBGI-SHENZHEN, Shenzhen, China.ORCID http://orcid.org/0000-0003-0342-9593
Meiqi WangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Hao LiuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Shanliang ZhengSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Olga BureninaCenter for Molecular and Cellular Biology, Skolkovo Institute of Science and Technology, Moscow, Russia.
Zhiyuan XiangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Li LiThe third affiliated hospital of Harbin Medical University, Harbin, China.
Jiaqi ZhuSchool of Astronautics, Harbin Institute of Technology, Harbin, China.
Ying HuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China. huying@hit.edu.cn.ORCID http://orcid.org/0000-0003-2469-5604

Funding

China Postdoctoral Science Foundation 2023M740931China Postdoctoral Science Foundation GZC20233466National Natural Science Foundation of China (National Science Foundation of China) 82403269National Science Foundation of China | Key Programme 82403269
6 · The paper itself

Abstract

Despite being hailed as a significant advancement in cancer treatment, immune checkpoint blockade (ICB) has not yielded favorable outcomes in colorectal cancer, both in approximately 85% of cases characterized by microsatellite stability (MSS) and approximately 50% of microsatellite instability (MSI) cases. How ICB efficiency in colorectal cancer treatment can be improved remains unclear. Here, we identify a new immunoregulatory long non-coding RNA (lncRNA) gene named lncRNA of IFN-γ-signaling suppressor (LISS). LISS expression is increased in colorectal cancers and is linked to poor prognosis, as well as a high CD8+ score. Functional studies reveal that LISS impairs T cell-mediated cytotoxicity, regardless of MSS/MSI status. Mechanistically, LISS interacts directly with the kinase regulatory domain in calmodulin-dependent kinase (CamK)IIγ through a microdomain containing two independent RNA stem-loops. This interaction prevents the binding and phosphorylation of its substrate signal transducer and activator of transcription1 (STAT1) at serine(S)727, a modification necessary for optimal activation of STAT1 and the subsequent major histocompatibility complex I (MHC-I) gene expression. Analysis of human colorectal cancer samples reveals significant inverse correlations between LISS and pS-STAT1 or MHC-I. The knock-in of LISS in intestinal epithelium promotes adenoma development in Apc

Indexed as

Colorectal NeoplasmsMicrosatellite InstabilityRNA, Long NoncodingSTAT1 Transcription FactorAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Gene Expression Regulation, NeoplasticHumansInterferon-gammaMiceCalcium-Calmodulin-Dependent Protein Kinase Type 2Interferon-gammaRNA, Long NoncodingSTAT1 protein, humanSTAT1 Transcription Factor

Identifiers

PMID42204133
PMCPMC13216641

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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.