Evidence map›Paper›PMID 32612115›Full record

ArticleCell death & disease2020

Chondroitin polymerizing factor (CHPF) promotes development of malignant melanoma through regulation of CDK1.

Wei Sun, Fang Zhao, Yu Xu, Kai Huang, Xianling Guo, Biqiang Zheng, Xin Liu, Zhiguo Luo, Yunyi Kong, Midie Xu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 22 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

12 authors at 4 institutions in 2 countries.

Wei Sun *Department of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Fang Zhao *Department of Dermatology, University Hospital Essen, Hufelandstrasse 55, 45122, Essen, Germany.
Yu Xu *Department of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Kai Huang *Brandon Reginal Hospital, HCA Healthcare/USF Morsani College of Medicine, Brandon, FL, USA.
Xianling Guo *Department of Oncology, Dermatology Hospital, Tongji University, Shanghai, China.
Biqiang ZhengDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Xin LiuDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Zhiguo LuoDepartment of Medical Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Yunyi KongDepartment of Pathology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Midie XuDepartment of Pathology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Dirk SchadendorfDepartment of Dermatology, University Hospital Essen, Hufelandstrasse 55, 45122, Essen, Germany. dirk.schadendorf@uk-essen.de.
Yong ChenDepartment of Musculoskeletal Oncology, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China. chenyong@fudan.edu.cn.
Fudan University Shanghai Cancer Center · CNEssen University Hospital · DEShanghai Medical College of Fudan University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chondroitin polymerizing factor (CHPF) is an important member of glycosyltransferases involved in the biosynthesis of chondroitin sulfate (CS). However, the relationship between CHPF and malignant melanoma (MM) is still unknown. In this study, it was demonstrated that CHPF was up-regulated in MM tissues compared with the adjacent normal skin tissues and its high expression was correlated with more advanced T stage. Further investigations indicated that the over-expression/knockdown of CHPF could promote/inhibit proliferation, colony formation and migration of MM cells, while inhibiting/promoting cell apoptosis. Moreover, knockdown of CHPF could also suppress tumorigenicity of MM cells in vivo. RNA-sequencing followed by Ingenuity pathway analysis (IPA) was performed for exploring downstream of CHPF and identified CDK1 as the potential target. Furthermore, our study revealed that knockdown of CDK1 could inhibit development of MM in vitro, and alleviate the CHPF over-expression induced promotion of MM. In conclusion, our study showed, as the first time, CHPF as a tumor promotor for MM, whose function was carried out probably through the regulation of CDK1.

Indexed as

ApoptosisCarcinogenesisCDC2 Protein KinaseCell Line, TumorCell MovementCell ProliferationDisease ProgressionEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansMaleMelanomaMiddle AgedN-AcetylgalactosaminyltransferasesCDC2 Protein KinaseCDK1 protein, humanchondroitin synthaseN-Acetylgalactosaminyltransferases

Identifiers

PMID32612115
PMCPMC7329816
OpenAlexW3039839774

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.