Evidence map›Paper›PMID 42251192›Full record

ArticleOncogene2026

LncRNA 606938-TFAM axis drives oxidative stress and activates cGAS-STING pathway-mediated antitumor immunity to restrain colorectal cancer progression.

Jin'e Du, Zhichao Guo, Qiao Lu, Huiqin Guo, Fengming Liu, Zhaoying Hao, Yiwei Duan, Zhuoyu Li, Haili Wu

Abstract read
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In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

9 authors.

Jin'e Du *Institute of Biotechnology, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China.
Zhichao GuoBiomedical and Health Laboratory in Shanxi Province, Taiyuan, China.
Qiao LuInstitute of Biotechnology, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China.
Huiqin GuoShanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi Medical University, Tongji Shanxi Hospital, Taiyuan, China.
Fengming LiuBiomedical and Health Laboratory in Shanxi Province, Taiyuan, China.
Zhaoying HaoCollege of Life Science, Shanxi University, Taiyuan, China.
Yiwei DuanInstitute of Biotechnology, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China.
Zhuoyu LiInstitute of Biotechnology, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China.
Haili Wu *Institute of Biotechnology, The Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education, Shanxi University, Taiyuan, China. whl@sxu.edu.cn.ORCID http://orcid.org/0000-0003-3338-7822

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82072718National Natural Science Foundation of China (National Science Foundation of China) U23A20526Shanxi Province Science Foundation for Youths 202203021222007
6 · The paper itself

Abstract

Colorectal cancer (CRC) remains the third most common malignancy and a leading cause of cancer-related mortality worldwide. Despite immunotherapy advances, most CRCs respond poorly to immune checkpoint inhibitors due to their immunologically "cold" phenotype characterized by low immunogenicity and a suppressive tumor microenvironment. Oxidative stress has emerged as a critical determinant of antitumor immunity, with excessive reactive oxygen species (ROS) triggering immunogenic cell death, releasing tumor-associated antigens and damage-associated molecular patterns. However, endogenous mechanisms linking ROS regulation to innate immune activation remain incompletely understood. Here, we identify a previously unreported mitochondria-associated long non-coding RNA, lncRNA 606938, whose expression is inversely correlated with CRC progression. Mechanistically, lncRNA 606938 is exported from the nucleus via the HuR-IGF2BP2 complex and translocated to mitochondria through the mitochondrial targeting sequence and HMG2 domains of mitochondrial transcription factor A (TFAM). Within mitochondria, lncRNA 606938 enhances oxidative phosphorylation (OXPHOS) by upregulating mitochondrial DNA-encoded OXPHOS subunits, leading to excessive ROS production. In addition, lncRNA 606938 facilitates the recognition of N6-methyladenosine (m

Indexed as

Colorectal NeoplasmsDNA-Binding ProteinsMembrane ProteinsMitochondrial ProteinsNucleotidyltransferasesOxidative StressRNA, Long NoncodingTranscription FactorsAnimalsCell Line, TumorcGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDisease ProgressionGene Expression Regulation, NeoplasticHumansImmunity, InnatecGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA-Binding ProteinsMembrane ProteinsMitochondrial ProteinsNucleotidyltransferasesReactive Oxygen SpeciesRNA, Long NoncodingSTING1 protein, humanSTING ProteinTranscription Factors

Identifiers

PMID42251192

What OpenQuestion holds

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Registered trials

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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.