Evidence map›Paper›PMID 31627350›Full record

ArticleCancers2019

CD200 Induces Epithelial-to-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma via β-Catenin-Mediated Nuclear Translocation.

Seung-Phil Shin, A-Ra Goh, Hyeon-Gu Kang, Seok-Jun Kim, Jong-Kwang Kim, Kyung-Tae Kim, John H Lee, Yong-Soo Bae, Yuh-Seog Jung, Sang-Jin Lee

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  4. Article
  5. Review
  6. AnCancer informatics · 2022
    Article
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  8. Article
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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

10 authors at 4 institutions in 2 countries.

Seung-Phil ShinDivision of Tumor Immunology, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. apollossp@ncc.re.kr.
A-Ra GohDivision of Tumor Immunology, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. ahra8714@naver.com.
Hyeon-Gu KangDepartment of Biomedical Science, BK21-Plus Research Team for Bioactive Control Technology, College of Natural Sciences, Chosun University, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Korea. kang84562@nate.com.
Seok-Jun KimDepartment of Biomedical Science, BK21-Plus Research Team for Bioactive Control Technology, College of Natural Sciences, Chosun University, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Korea. heaven1472@chosun.ac.kr.
Jong-Kwang KimGenome Analysis Team, Research Core Center, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. jk@ncc.re.kr.ORCID 0000-0001-9290-0820
Kyung-Tae KimDivision of Cancer Biology, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. bioktkim@ncc.re.kr.
John H LeeAdult Medical Affairs, NantKwest, 9020 Jefferson Blvd, Culver City, CA 90232, USA. john.lee@nantkwest.com.
Yong-Soo BaeDepartment of Biological Sciences, SRC Center for Immune Research on Non-lymphoid Organs, Sungkyunkwan University, Jangan-gu, Suwon 16419, Korea. ysbae04@skku.edu.ORCID 0000-0002-2233-9449
Yuh-Seog JungDivision of Tumor Immunology, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. jysorl@ncc.re.kr.
Sang-Jin LeeDivision of Tumor Immunology, Research Institute & Hospital, National Cancer Center, Goyang 10408, Korea. leesj@ncc.re.kr.
National Cancer Center · KRChosun University · KRImmunityBio (United States) · USSungkyunkwan University · KR

Funding

National Cancer Center, Korea NCC-1910010
6 · The paper itself

Abstract

The membrane glycoprotein CD200 binds to its receptor CD200R1 and induces tolerance, mainly in cells of the myeloid lineage; however, information regarding its role in solid tumors is limited. Here, we investigated whether CD200 expression, which is enriched mainly in high-grade head and neck squamous cell carcinoma (HNSCC), correlates with cancer progression, particularly the epithelial-to-mesenchymal transition (EMT). The forced overexpression of CD200 in the HNSCC cell line, UMSCC84, not only increased the expression of EMT-related genes, but also enhanced invasiveness. The cleaved cytoplasmic domain of CD200 interacted with β-catenin in the cytosol, was translocated to the nucleus, and eventually enhanced EMT-related gene expression. CD200 increased the invasiveness of mouse tonsillar epithelium immortalized with E6, E7, and Ras (MEER), a model of tonsillar squamous cell carcinoma. siRNA inhibition of CD200 or extracellular domain of CD200R1 down-regulated the expression of EMT-related genes and decreased invasiveness. Consistently, compared to CD200-null MEER tumors, subcutaneous CD200-expressing MEER tumors showed significantly increased metastatic migration into draining lymph nodes. Our study demonstrates a novel and unique role of CD200 in inducing EMT, suggesting the potential therapeutic target for blocking solid cancer progression.

Indexed as

CD200EMTHNSCCβ-catenin

Identifiers

PMID31627350
PMCPMC6826410
OpenAlexW2980978993

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.