Evidence map›Paper›PMID 41285764›Full record

ArticleCell death discovery2025

hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability.

Kai Ji, Leqi Zhou, Tianshuai Zhang, Hao Fan, Gang Xie, Wenjiang Man, Can Wang, Yucheng Tian, Li Chen, Guimin Wang and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2025. 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

14 authors.

Kai Ji *Department of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Leqi Zhou *Department of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Tianshuai Zhang *Department of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Hao FanDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Gang XieDepartment of Anorectal Surgery, Huaibei People's Hospital, Huaibei, Anhui, China.
Wenjiang ManDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Can WangDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Yucheng TianDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Li ChenDepartment of Anorectal Surgery, Huaibei People's Hospital, Huaibei, Anhui, China.
Guimin WangDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China.
Mulin LiuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China.
Bing ZhuDepartment of Gastrointestinal Surgery, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China. bbmczhubing@163.com.ORCID http://orcid.org/0000-0003-4165-2120
Wei ZhangDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China. weizhang2000cn@163.com.ORCID http://orcid.org/0000-0003-3094-9711
Guanyu YuDepartment of Colorectal Surgery, Shanghai Changhai Hospital, Naval Medical University, Shanghai, China. yuguanyu0451@163.com.ORCID http://orcid.org/0000-0001-5416-3559

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence indicates that RNA-binding proteins and the reprogramming of lipid metabolism play crucial roles in tumorigenesis. However, the extent to which members of these families contribute, and whether targeting metabolic genes to affect overall protein production in cancer cells, remains largely unknown. This study analyzes CRC tissue samples and databases to reveal the high expression of hnRNP A1 in CRC and its critical role in tumorigenesis, proliferation, migration, and prognosis. Through combined sequencing analyses, we identified a novel mechanism by which PPARα regulates lipid metabolism. Our data indicate that hnRNP A1 is central to lipid metabolism reprogramming in CRC, promoting lipid accumulation by regulating PPARα mRNA stability, thereby influencing cell proliferation and apoptosis. Overall, hnRNP A1 could serve as a novel target for CRC therapy. Its involvement in cancer development offers new biological insights and potential therapeutic strategies. As a potential biomarker and therapeutic target, it presents novel approaches for the clinical management of CRC.

Identifiers

PMID41285764
PMCPMC12644753

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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.