Evidence map›Paper›PMID 42587760›Full record

ArticleCells2026

The LINC02041/SRSF1 Axis Facilitates Aerobic Glycolysis and Stemness Maintenance in Hepatocellular Carcinoma.

Mingjiao Cheng, Anqi Cheng, Chenglong Li, Zhibiao Zhang, Tingjiang He, Ludan Zhang, Qianwei Zhao, Jingjing Liu, Weiwei Lin, Jintao Zhang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 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
–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

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

11 authors.

Mingjiao ChengHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Anqi ChengHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Chenglong LiHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Zhibiao ZhangAcademy of Medical Engineering and Translational Medicine, Tianjin University, Tianjin 300072, China.
Tingjiang HeHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Ludan ZhangHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Qianwei ZhaoHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Jingjing LiuHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.ORCID 0000-0002-7965-3332
Weiwei LinHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.ORCID 0000-0001-7894-5408
Jintao ZhangHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.
Fang XuHenan Institute of Medical and Pharmaceutical Sciences, Zhengzhou University, Zhengzhou 450052, China.ORCID 0000-0002-5722-0798

Funding

Henan Science and Technology Department No.262102310156, No. 252102310154, No. 252102310300
6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) remains one of the most aggressive and lethal malignancies worldwide, with high rates of metastasis and recurrence contributing to its poor prognosis. There is an urgent need to elucidate the molecular mechanisms driving HCC progression and to develop effective therapeutic strategies. Metabolic reprogramming, especially aerobic glycolysis known as the Warburg effect, is a well-established hallmark of cancer. Concurrently, cancer stem cells (CSCs) play crucial roles in tumor initiation, therapy resistance, and recurrence. However, the involvement of long non-coding RNAs (lncRNAs) in linking metabolic alterations and stemness remains poorly understood. In this investigation, we identified LINC02041 as a significantly upregulated lncRNA in HCC tissues and demonstrated its oncogenic role in promoting cell proliferation. We found that STAT3 transcriptionally activates LINC02041 expression. Mechanistically, LINC02041 enhances the stability of SRSF1 protein by suppressing its ubiquitin-mediated degradation, thereby facilitating HCC cell proliferation, migration, glycolytic metabolism, and acquisition of stem-like properties. Our findings delineate a novel STAT3/LINC02041/SRSF1 regulatory axis that coordinately modulates glycolytic reprogramming and stemness maintenance in hepatocarcinogenesis. This study not only advances our understanding of HCC pathophysiology but also identifies LINC02041 as a promising prognostic biomarker and a compelling therapeutic target for novel therapeutic strategies against this aggressive malignancy.

Indexed as

Carcinoma, HepatocellularGlycolysisLiver NeoplasmsNeoplastic Stem CellsRNA, Long NoncodingAnimalsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansMetabolic ReprogrammingSTAT3 Transcription FactorRNA, Long NoncodingSTAT3 Transcription FactorglycolysisHCCLINC02041SRSF1STAT3stemness

Identifiers

PMID42587760
PMCPMC13465720

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.