Evidence map›Paper›PMID 33050232›Full record

ArticleCancers2020

CD99-PTPN12 Axis Suppresses Actin Cytoskeleton-Mediated Dimerization of Epidermal Growth Factor Receptor.

Kyoung-Jin Lee, Yuri Kim, Min Seo Kim, Hyun-Mi Ju, Boyoung Choi, Hansoo Lee, Dooil Jeoung, Ki-Won Moon, Dongmin Kang, Jiwon Choi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  6. Review
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 1 country.

Kyoung-Jin LeeDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Yuri KimDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Min Seo KimDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Hyun-Mi JuDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Boyoung ChoiDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Hansoo LeeDepartment of Biological Sciences, College of Natural Sciences, Kangwon National University, Chuncheon 24341, Korea.
Dooil JeoungDepartment of Biochemistry, College of Natural Sciences, Kangwon National University, Chuncheon 24341, Korea.
Ki-Won MoonDepartment of Rheumatology, Kangwon National University Hospital, Chuncheon 24289, Korea.
Dongmin KangDepartment of Life Science, Ewha Womans University, Seoul 03760, Korea.ORCID 0000-0001-5997-625X
Jiwon ChoiMet Life Sciences Co., Ltd., Seoul 03722, Korea.
Jong In YookMet Life Sciences Co., Ltd., Seoul 03722, Korea.ORCID 0000-0002-7318-6112
Jang-Hee HahnDepartment of Anatomy and Cell Biology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Kangwon National University · KRYonsei University · KREwha Womans University · KRKangwon National University Hospital · KR

Funding

Kangwon National University No. 520170543National Research Foundation of Korea 2018R1D1A3B07043170
6 · The paper itself

Abstract

The epidermal growth factor receptor (EGFR), a member of ErbB receptor tyrosine kinase (RTK) family, is activated through growth factor-induced reorganization of the actin cytoskeleton and subsequent dimerization. We herein explored the molecular mechanism underlying the suppression of ligand-induced EGFR dimerization by CD99 agonists and its relevance to tumor growth in vivo. Epidermal growth factor (EGF) activated the formation of c-Src/focal adhesion kinase (FAK)-mediated intracellular complex and subsequently induced RhoA-and Rac1-mediated actin remodeling, resulting in EGFR dimerization and endocytosis. In contrast, CD99 agonist facilitated FAK dephosphorylation through the HRAS/ERK/PTPN12 signaling pathway, leading to inhibition of actin cytoskeletal reorganization via inactivation of the RhoA and Rac1 signaling pathways. Moreover, CD99 agonist significantly suppressed tumor growth in a BALB/c mouse model injected with MDA-MB-231 human breast cancer cells. Taken together, these results indicate that CD99-derived agonist ligand inhibits epidermal growth factor (EGF)-induced EGFR dimerization through impairment of cytoskeletal reorganization by PTPN12-dependent c-Src/FAK inactivation, thereby suppressing breast cancer growth.

Indexed as

actin cytoskeletal reorganizationbreast cancerCD99 agonistEGFR dimerizationendocytosisFAK dephosphorylationPTPN12Rac1RhoAtripeptide

Identifiers

PMID33050232
PMCPMC7599698
OpenAlexW3092029458

What Socratic 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 Socratic graph.