Evidence map›Paper›PMID 32273729›Full record

ArticleOncoTargets and therapy2020

Fibroblast Activation Protein (FAP) Overexpression Induces Epithelial-Mesenchymal Transition (EMT) in Oral Squamous Cell Carcinoma by Down-Regulating Dipeptidyl Peptidase 9 (DPP9).

Qing-Qing Wu, Meng Zhao, Guang-Zhao Huang, Ze-Nan Zheng, Yuechuan Chen, Wei-Sen Zeng, Xiao-Zhi Lv

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Beta-endoproteolysis of the cellular prion protein by dipeptidyl peptidase-4 and fibroblast activation protein.Proceedings of the National Academy of Sciences of the United States of America · 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

7 authors at 1 institution in 1 country.

Qing-Qing WuDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.ORCID 0000-0002-8931-3630
Meng ZhaoDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Guang-Zhao HuangDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Ze-Nan ZhengDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Yuechuan ChenDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Wei-Sen ZengDepartment of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou, People's Republic of China.
Xiao-Zhi LvDepartment of Oral & Maxillofacial Surgery, NanFang Hospital, Southern Medical University, Guangzhou, People's Republic of China.
Southern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeFibroblast activation protein (FAP) acts as a tumor promoter via epithelial-mesenchymal transition (EMT) in human oral squamous cell carcinoma (OSCC). The present study was designed to investigate the FAP targeting proteins and explore the precise mechanism by which FAP promotes EMT in OSCC. PATIENTS AND

methodsProteins interacting with FAP were found and filtered by immunoprecipitation-mass spectrometry (IP-MS). Both DPP9 protein and mRNA were examined in 90 paired OSCC samples and matched normal tissue. DPP9 knockdown was conducted to determine its function in OSCC in vitro and in vivo.

resultsDipeptidyl peptidase 9 (DPP9) was identified as interacting with FAP intracellularly by IP-MS. The levels of both DPP9 protein and mRNA were down-regulated in OSCC tissue. Lower DPP9 expression was correlated with unfavorable survival rates of OSCC patients. DPP9 knockdown accelerates the proliferation of OSCC cells in vitro and in vivo. Overexpression of FAP leads to a reduction in DPP9 expression. Likewise, DPP9 overexpression reverses the proliferation, migration, invasion and EMT induced by FAP during OSCC.

conclusionOur study finds that FAP promotes EMT of OSCC by down-regulating DPP9 in a non-enzymatic manner. FAP-DPP9 pathway could be a potential therapeutic target of OSCC.

Indexed as

DPP9EMTFAPoral cancerOSCC

Identifiers

PMID32273729
PMCPMC7113806
OpenAlexW3013793544

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.