Evidence map›Paper›PMID 41691251›Full record

ArticleMolecular cancer2026

FBXW7 mutations reprogram glucose metabolism by activating the ETV6-GLUT1 axis.

Siqi Fei, Xiayun Xu, Tingrui Wang, Xinyue Jiang, Hanrong Zhu, Yingji Chen, Renjie Yuan, Zeheng Lv, Zhijian Gao, Huanxin Liu and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cancer, 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

13 authors.

Siqi Fei *Department of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, P.R. China.
Xiayun Xu *Shanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Tingrui WangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Xinyue JiangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Hanrong ZhuShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Yingji ChenShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Renjie YuanDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, P.R. China.
Zeheng LvDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, P.R. China.
Zhijian GaoShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Huanxin LiuShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China.
Xiaojun ChenDepartment of Gynecology, the Tenth People's Hospital of Tongji University, Shanghai, 200072, P.R. China.
Chenji WangShanghai Pudong Hospital, Fudan University Pudong Medical Center, State Key Laboratory of Genetics and Development of Complex Phenotypes, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, 200438, P.R. China. chenjiwang@fudan.edu.cn.
Kun GaoDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, P.R. China. kungao@tongji.edu.cn.

Funding

China Postdoctoral Science Foundation GZC20240296National Natural Science Foundation of China 82573799National Natural Science Foundation of China 92357301Natural Science Foundation of Shanghai 22ZR1406600Natural Science Foundation of Shanghai Municipality 22ZR1449200Open Research Fund of Shanghai Key Laboratory of Maternal and Fetal Medicine, mfmkf202204Seed Program for Research and Translation of New Medical Technologies 2024ZZ2016State Key Development Programs of China 2022YFA1104200
6 · The paper itself

Abstract

The progression of endometrial cancer (EC) involves substantial metabolic reprogramming, frequently driven by mutations in tumor suppressors and oncogenes. In this study, we identify a previously unrecognized pathway through which FBXW7 mutations rewire glucose metabolism in EC cells. Specifically, we demonstrate that loss-of-function mutations in FBXW7 disrupt the SCF

Indexed as

Endometrial NeoplasmsF-Box-WD Repeat-Containing Protein 7GlucoseGlucose Transporter Type 1MutationProto-Oncogene Proteins c-etsRepressor ProteinsAnimalsCell Line, TumorCell ProliferationETS Translocation Variant 6 ProteinFemaleGene Expression Regulation, NeoplasticHumansMetabolic ReprogrammingSignal TransductionETS Translocation Variant 6 ProteinF-Box-WD Repeat-Containing Protein 7FBXW7 protein, humanGlucoseGlucose Transporter Type 1Proto-Oncogene Proteins c-etsRepressor ProteinsSLC2A1 protein, humanEndometrial cancerFBXW7Glucose metabolismUbiquitination

Identifiers

PMID41691251
PMCPMC13011662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.