Evidence map›Paper›PMID 42009961›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2026

METTL7A inhibits progression of colorectal cancer through the SREBP1 / FDFT1 / SQLE / CYP51A1 / cholesterol metabolic pathway.

Sha Li, Xiangyin Chi, Xiaoxue Li, Wan Li, Hong Yang, Wanxin Cao, Yuxuan Zhao, Xu Zhang, Rui Meng, Guanhua Du and 2 more

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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

The trial behind it

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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

12 authors.

Sha Li *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Xiangyin Chi *State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Xiaoxue LiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Wan LiState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Hong YangState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Wanxin CaoState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Yuxuan ZhaoState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Xu ZhangState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Rui MengState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Guanhua DuState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China.
Dan ZhangState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China. danzhang@imm.ac.cn.
Jinhua WangState Key Laboratory of Bioactive Substance and Function of Natural Medicines, Beijing, 100050, China. wjh@imm.ac.cn.

Funding

Beijing Natural Science Foundation 7252202, 25JL008CAMS Innovation Fund for Medical Sciences 2021-I2M-1-029Inner Mongolian Natural Science Foundation 2024MS08023
6 · The paper itself

Abstract

backgroundColorectal cancer (CRC) incidence and mortality rates are steadily on the rise, which brings significant public health concern worldwide, especially in China. Methyltransferase-like 7 A (METTL7A), a member of the methyltransferase-like family, is associated with various cancers including CRC. Notably, CRC progression is closely linked to metabolic reprogramming. However, its precise role in CRC, particularly metabolic reprogramming of CRC, remains unclear.

methodsMETTL7A was identified as a pivotal gene closely associated with CRC by bioinformatics analyses. Through a series of cellular functional assays and several animal experiments, such as in situ tumor and spontaneous tumor in C57BL/6 mice, the role of METTL7A in the development of colorectal cancer was evaluated. Transcriptomics and proteomics were used to analyze the effects of METTL7A on the expression of numerous genes, especially those involved in metabolic processes including cholesterol synthesis pathway within CRC cells. Western-blotting, co-immunoprecipitation and immunofluorescence were used to elucidate the relationship of METTL7A and the cholesterol metabolic pathway.

resultsMETTL7A exhibited low expression in CRC cell lines and CRC tissues and it was demonstrated to function as a tumor suppressor in CRC. Transcriptomic and proteomic analyses indicated that METTL7A affects genes related to the cholesterol metabolism pathway. METTL7A was further proven to directly bind to Sterol Regulatory Element-Binding Protein1 (SREBP1) and SREBP Cleavage-Activating Protein (SCAP), hindering the nuclear translocation of SREBP1 and thereby reducing intracellular cholesterol content.

conclusionsThis study provides valuable insights into the role of METTL7A in CRC and its impact on metabolic reprogramming, particularly cholesterol synthesis, and identifies METTL7A as a potential therapeutic target of CRC.

Indexed as

CholesterolColorectal NeoplasmsDisease ProgressionMetabolic Networks and PathwaysMethyltransferasesSterol Regulatory Element Binding Protein 1AnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMetabolic ReprogrammingMiceMice, Inbred C57BLCholesterolMethyltransferasesSterol Regulatory Element Binding Protein 1Cholesterol synthesisCRCMetabolic reprogrammingMETTL7ASREBP1

Identifiers

PMID42009961
PMCPMC13096364

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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.