Evidence map›Paper›PMID 31969394›Full record

ArticleThe Journal of biological chemistry2020

Extracellular Domains I and II of cell-surface glycoprotein CD44 mediate its

Madoka Kawaguchi, Nurmaa Dashzeveg, Yue Cao, Yuzhi Jia, Xia Liu, Yang Shen, Huiping Liu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 38 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

7 authors at 3 institutions in 2 countries.

Madoka KawaguchiDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; Laboratory of Functional Biology, Graduate School of Biostudies, Kyoto University, Kyoto, 6068501, Japan.
Nurmaa DashzevegDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.
Yue CaoDepartment of Electrical and Computer Engineering, TEES-AgriLife Center for Bioinformatics and Genomic Systems Engineering, Texas A&M University, College Station, Texas 77843.
Yuzhi JiaDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611.
Xia LiuDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; Department of Toxicology and Cancer Biology, College of Medicine, University of Kentucky, Lexington, Kentucky 40536. Electronic address: xli369@uky.edu.
Yang ShenDepartment of Electrical and Computer Engineering, TEES-AgriLife Center for Bioinformatics and Genomic Systems Engineering, Texas A&M University, College Station, Texas 77843. Electronic address: YShen@tamu.edu.
Huiping LiuDepartment of Pharmacology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; Department of Medicine, Hematology/Oncology Division, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; Robert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611. Electronic address: huiping.liu@northwestern.edu.
Northwestern University · USTexas A&M University · USTexas A&M University System · US

Funding

Unraveling molecular and system-level mechanisms of human disease-associated protein mutationsR35GM124952 · NIGMS · TEXAS ENGINEERING EXPERIMENT STATION · PI Yang Shen · 2017 to 2026
$2.9M
Molecular mechanisms underlying circulating tumor cell aggregationR01CA245699 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LIU, HUIPING · 2020 to 2024
$2.0M
Identifying a network of miRNAs and genes that regulate breast tumor metastasisR00CA160638 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LIU, HUIPING · 2014 to 2017
$883k
NCI NIH HHS R00 CA160638NCI NIH HHS R01 CA245699NIGMS NIH HHS R35 GM124952
6 · The paper itself

Abstract

CD44 molecule (CD44) is a well-known surface glycoprotein on tumor-initiating cells or cancer stem cells. However, its utility as a therapeutic target for managing metastases remains to be fully evaluated. We previously demonstrated that CD44 mediates homophilic interactions for circulating tumor cell (CTC) cluster formation, which enhances cancer stemness and metastatic potential in association with an unfavorable prognosis. Furthermore, CD44 self-interactions activate the P21-activated kinase 2 (PAK2) signaling pathway. Here, we further examined the biochemical properties of CD44 in homotypic tumor cell aggregation. The standard CD44 form (CD44s) mainly assembled as intercellular homodimers (

Indexed as

Cell AggregationAmino Acid SubstitutionAnimalsDimerizationHumansHyaluronan ReceptorsMiceNeoplasm MetastasisNeoplasmsNeoplastic Stem Cellsp21-Activated KinasesProtein DomainsCD44 protein, humanHyaluronan Receptorsp21-Activated KinasescancerCD44cell-cell aggregationcirculating tumor cellhomophilic interactionsmachine learningmetastasismutagenesisP21-activated kinase 2 (PAK2)protein dockingprotein domainprotein-protein interactiontumor cell cluster

Identifiers

PMID31969394
PMCPMC7049959
OpenAlexW3001030586

What OpenQuestion holds

Textmetadata
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.