Evidence map›Paper›PMID 32313017›Full record

ArticleNature communications2020

Fasting inhibits aerobic glycolysis and proliferation in colorectal cancer via the Fdft1-mediated AKT/mTOR/HIF1α pathway suppression.

Mei-Lin Weng, Wan-Kun Chen, Xiang-Yuan Chen, Hong Lu, Zhi-Rong Sun, Qi Yu, Peng-Fei Sun, Ya-Jun Xu, Min-Min Zhu, Nan Jiang and 6 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 162 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
162citing papers in PubMed, 1 pooled it
12.0field-weighted citation impact, top 1% of its field
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

162 citing papers in PubMed, 1 synthesis or guideline pooled it, 249 citations in OpenAlex.

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102 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Mei-Lin Weng *Department of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Wan-Kun Chen *Department of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.ORCID http://orcid.org/0000-0001-7394-9266
Xiang-Yuan Chen *Department of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Hong LuDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Zhi-Rong SunDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Qi YuDepartment of Radiation Oncology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Peng-Fei SunDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Ya-Jun XuDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Min-Min ZhuDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Nan JiangKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Collaborative Innovation Center of Genetics and Development, Institutes of Biomedical Science, School of Basic Medical Science, Fudan University, Shanghai, 200032, China.
Jin ZhangKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Collaborative Innovation Center of Genetics and Development, Institutes of Biomedical Science, School of Basic Medical Science, Fudan University, Shanghai, 200032, China.
Jian-Ping ZhangInstitute of Modern Physics, Fudan University; Department of Nuclear Medicine, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China.
Yuan-Lin SongDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Duan MaKey Laboratory of Metabolism and Molecular Medicine, Ministry of Education, Department of Biochemistry and Molecular Biology, Collaborative Innovation Center of Genetics and Development, Institutes of Biomedical Science, School of Basic Medical Science, Fudan University, Shanghai, 200032, China. duanma@fudan.edu.cn.
Xiao-Ping ZhangThe Institute of Intervention Vessel, Tongji University School of Medicine, Shanghai, 200092, China. zxpsibs@163.com.
Chang-Hong MiaoDepartment of Anesthesiology, Fudan University Shanghai Cancer Center; Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 200032, China. whitedolphin2007@hotmail.com.ORCID http://orcid.org/0000-0002-4730-1201
Shanghai Medical College of Fudan University · CNFudan University · CNSun Yat-sen University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evidence suggests that fasting exerts extensive antitumor effects in various cancers, including colorectal cancer (CRC). However, the mechanism behind this response is unclear. We investigate the effect of fasting on glucose metabolism and malignancy in CRC. We find that fasting upregulates the expression of a cholesterogenic gene, Farnesyl-Diphosphate Farnesyltransferase 1 (FDFT1), during the inhibition of CRC cell aerobic glycolysis and proliferation. In addition, the downregulation of FDFT1 is correlated with malignant progression and poor prognosis in CRC. Moreover, FDFT1 acts as a critical tumor suppressor in CRC. Mechanistically, FDFT1 performs its tumor-inhibitory function by negatively regulating AKT/mTOR/HIF1α signaling. Furthermore, mTOR inhibitor can synergize with fasting in inhibiting the proliferation of CRC. These results indicate that FDFT1 is a key downstream target of the fasting response and may be involved in CRC cell glucose metabolism. Our results suggest therapeutic implications in CRC and potential crosstalk between a cholesterogenic gene and glycolysis.

Indexed as

AnimalsCell Line, TumorCell ProliferationColonic NeoplasmsColorectal NeoplasmsDisease Models, AnimalDown-RegulationFarnesyl-Diphosphate FarnesyltransferaseFastingFemaleGlycolysisHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMice, Inbred BALB CMiddle AgedFarnesyl-Diphosphate FarnesyltransferaseHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMTOR protein, humanProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID32313017
PMCPMC7170903
OpenAlexW3017148053

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.