Evidence map›Paper›PMID 30385854›Full record

ArticleOncogene2019

Bioinformatics-based analysis reveals elevated MFSD12 as a key promoter of cell proliferation and a potential therapeutic target in melanoma.

Chuan-Yuan Wei, Meng-Xuan Zhu, Nan-Hang Lu, Rui Peng, Xuan Yang, Peng-Fei Zhang, Lu Wang, Jian-Ying Gu

Open access · greenAbstract read
In one paragraph

Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 5% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.

  1. Pooled it
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  17. Lysosomal lipid peroxidation regulates tumor immunity.The Journal of clinical investigation · 2023
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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

8 authors at 4 institutions in 1 country.

Chuan-Yuan WeiDepartment of Plastic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Meng-Xuan ZhuLiver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Shanghai, 200032, People's Republic of China.
Nan-Hang LuDepartment of Plastic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Rui PengLiver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Shanghai, 200032, People's Republic of China.
Xuan YangLiver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Shanghai, 200032, People's Republic of China.
Peng-Fei ZhangLiver Cancer Institute, Zhongshan Hospital, Fudan University; Key Laboratory of Carcinogenesis and Cancer Invasion (Fudan University), Ministry of Education, Shanghai, 200032, People's Republic of China.
Lu WangDepartment of Plastic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China.
Jian-Ying GuDepartment of Plastic Surgery, Zhongshan Hospital, Fudan University, Shanghai, 200032, People's Republic of China. zhongshanhospital@163.com.
Fudan University · CNSun Yat-sen University · CNZhongshan Hospital · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) G2016--23
6 · The paper itself

Abstract

Although recent therapeutic advances based on our understanding of molecular phenomena have prolonged the survival of melanoma patients, the prognosis of melanoma remains dismal and further understanding of the underlying mechanism of melanoma progression is needed. In this study, differential expression analyses revealed that many genes, including AKT1 and CDK2, play important roles in melanoma. Functional analyses of differentially expressed genes (DEGs), obtained from the GEO (Gene Expression Omnibus) database, indicated that high proliferative and metastatic abilities are the main characteristics of melanoma and that the PI3K and MAPK pathways play essential roles in melanoma progression. Among these DEGs, major facilitator superfamily domain-containing 12 (MFSD12) was found to have significantly and specifically upregulated expression in melanoma, and elevated MFSD12 level promoted cell proliferation by promoting cell cycle progression. Mechanistically, MFSD12 upregulation was found to activate PI3K signaling, and a PI3K inhibitor reversed the increase in cell proliferation endowed by MFSD12 upregulation. Clinically, high MFSD12 expression was positively associated with shorter overall survival (OS) and disease-free survival (DFS) in melanoma patients, and MFSD12 was an independent prognostic factor for OS and DFS in melanoma patients. Therapeutically, in vivo assays further confirmed that MFSD12 interference inhibited tumor growth and lung metastasis in melanoma. In conclusion, elevated MFSD12 expression promotes melanoma cell proliferation, and MFSD12 is a valuable prognostic biomarker and promising therapeutic target in melanoma.

Indexed as

AdultAgedAged, 80 and overBiomarkers, TumorCell ProliferationCells, CulturedCell Transformation, NeoplasticComputational BiologyDisease ProgressionFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMelanomaMembrane ProteinsBiomarkers, TumorMembrane ProteinsMFSD12 protein, human

Identifiers

PMID30385854
PMCPMC6462865
OpenAlexW2898709937

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LicenceCC BY
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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.