Evidence map›Paper›PMID 28501528›Full record

ArticleEBioMedicine2017

BCKDK of BCAA Catabolism Cross-talking With the MAPK Pathway Promotes Tumorigenesis of Colorectal Cancer.

Peipei Xue, Fanfan Zeng, Qiuhong Duan, Juanjuan Xiao, Lin Liu, Ping Yuan, Linni Fan, Huimin Sun, Olesya S Malyarenko, Hui Lu and 8 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
0.8field-weighted citation impact, top 32% 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

43 citing papers in PubMed, 88 citations in OpenAlex.

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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

18 authors at 4 institutions in 2 countries.

Peipei XueDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Fanfan ZengDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Qiuhong DuanDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Juanjuan XiaoDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Lin LiuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Ping YuanDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Linni FanDepartment of Pathology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China.
Huimin SunDepartment of Urology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China.
Olesya S MalyarenkoDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China; G.B. Elyakov Pacific Institute of Bioorganic Chemistry, Far Eastern Branch of Russian Academy of Sciences, Laboratory of Enzyme Chemistry, Vladivostok, Russia.
Hui LuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Ruijuan XiuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Shaoqing LiuDepartment of State Key Laboratory of Cancer Biology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China.
Chen ShaoDepartment of Urology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China.
Jianmin ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.
Wei YanDepartment of Pathology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China. Electronic address: yan070@sina.com.
Zhe WangDepartment of Pathology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China. Electronic address: zhwang@fmmu.edu.cn.
Jianyong ZhengDepartment of State Key Laboratory of Cancer Biology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi 710032, PR China. Electronic address: zhengjy@fmmu.edu.cn.
Feng ZhuDepartment of Biochemistry and Molecular Biology, School of Basic Medicine, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China. Electronic address: fengzhu@hust.edu.cn.
Huazhong University of Science and Technology · CNXijing Hospital · CNAir Force Medical University · CNPacific Institute of Bioorganic Chemistry. GB Elyakova Far Eastern Branch of the Russian Academy of Sciences · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Branched-chain amino acids catabolism plays an important role in human cancers. Colorectal cancer is the third most commonly diagnosed cancer in males and the second in females, and the new global incidence is over 1.2 million cases. The branched-chain α-keto acid dehydrogenase kinase (BCKDK) is a rate-limiting enzyme in branched-chain amino acids catabolism, which plays an important role in many serious human diseases. Here we investigated that abnormal branched-chain amino acids catabolism in colorectal cancer is a result of the disease process, with no role in disease initiation; BCKDK is widely expressed in colorectal cancer patients, and those patients that express higher levels of BCKDK have shorter survival times than those with lower levels; BCKDK promotes cell transformation or colorectal cancer ex vivo or in vivo. Mechanistically, BCKDK promotes colorectal cancer by enhancing the MAPK signaling pathway through direct MEK phosphorylation, rather than by branched-chain amino acids catabolism. And the process above could be inhibited by a BCKDK inhibitor, phenyl butyrate.

Indexed as

MAP Kinase Signaling SystemAmino Acids, Branched-ChainAnimalsCell Line, TumorCell Transformation, NeoplasticColorectal NeoplasmsDisease Models, AnimalGene ExpressionHumansMaleMAP Kinase Kinase 1MicePhosphorylationPrognosisProtein Kinase InhibitorsProtein Kinases(3-methyl-2-oxobutanoate dehydrogenase (lipoamide)) kinaseAmino Acids, Branched-ChainMAP2K1 protein, humanMAP Kinase Kinase 1Protein Kinase InhibitorsProtein KinasesBCKDKBranched-chain amino acids catabolismColorectal cancerMEKPhenyl butyrateTumorigenesis

Identifiers

PMID28501528
PMCPMC5478211
OpenAlexW2611819331

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.