Evidence map›Paper›PMID 41685168›Full record

ArticleActa pharmaceutica Sinica. B2026

REEP6 promotes colorectal cancer glycolysis and tumorigenesis through PRMT5-mediated PGAM1 arginine methylation.

Tuo Wang, Dongsheng Zhang, Chi Jin, Hengjie Xu, Hongxu Nie, Ye Wang, Chuan Zhang, Yifei Feng, Junwei Tang, Yueming Sun

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta pharmaceutica Sinica. B, 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

10 authors.

Tuo WangDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Dongsheng ZhangDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Chi JinDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Hengjie XuDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Hongxu NieDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Ye WangDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Chuan ZhangDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yifei FengDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Junwei TangDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.
Yueming SunDepartment of General Surgery, Colorectal Institute of Nanjing Medical University, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic reprogramming is a notable hallmark of cancer biology, especially aerobic glycolysis. Some clinical trials attempt to target cancer metabolism to develop therapeutic agents. However, the results have been not satisfactory. Here, we report that REEP6 is significantly upregulated and promotes glycolysis and tumorigenesis in CRC. Moreover, REEP6, as a molecular scaffolder, bridges the PRMT5-PGAM1 complex, which enhances the PRMT5-mediated symmetric dimethylarginine (SDMA) of PGAM1 at R40. The methylated PGAM1 possesses dramatically enhanced enzymatic activity and therefore boosts glycolytic flux in CRC cells. More than that, our results showed that combined treatment with specific shRNA and inhibitors exhibits synergistic anti-tumor efficacy in CRC, which may shed light on the development of a promising therapy in CRC.

Indexed as

Aerobic glycolysisColorectal cancerMetabolic reprogrammingPGAM1PRMT5REEP6Symmetric dimethylarginineTumorigenesis

Identifiers

PMID41685168
PMCPMC12891873

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.