Evidence map›Paper›PMID 32816855›Full record

ReviewCancer research2020

Junctional Adhesion Molecules in Cancer: A Paradigm for the Diverse Functions of Cell-Cell Interactions in Tumor Progression.

Adam Lauko, Zhaomei Mu, David H Gutmann, Ulhas P Naik, Justin D Lathia

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.3field-weighted citation impact, top 3% 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, 74 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Review
  8. Junctional adhesion molecule-C: A multifunctional mediator of cell adhesion.Cellular and molecular life sciences : CMLS · 2025
    Review
  9. Article
  10. Epigenetic silencing ofOncology reports · 2025
    Article
  11. Review
  12. Article
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  17. Review
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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

5 authors at 4 institutions in 1 country.

Adam Lauko *Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.ORCID 0000-0001-5654-0784
Zhaomei Mu *Cardeza Center for Vascular Biology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania.
David H GutmannWashington University School of Medicine, St. Louis, Missouri.ORCID 0000-0002-3127-5045
Ulhas P Naik *Cardeza Center for Vascular Biology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania. lathiaj@ccf.org Ulhas.Naik@jefferson.edu.ORCID 0000-0001-7556-444X
Justin D Lathia *Department of Cardiovascular and Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio. lathiaj@ccf.org Ulhas.Naik@jefferson.edu.
Thomas Jefferson University · USCleveland Clinic · USCleveland Clinic Lerner College of Medicine · USWashington University in St. Louis · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007250 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI HUANG, ALEX YEE-CHEN · 1985 to 2023
$33.4M
Endogenous suppression of integrin signalingR01HL119374 · NHLBI · UNIVERSITY OF DELAWARE · PI NAIK, ULHAS P · 2013 to 2022
$3.8M
Novel adhesion mechanisms in glioblastoma stem cellsR01NS083629 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LATHIA, JUSTIN D. · 2013 to 2017
$1.7M
Connexins and glioblastoma progressionR01NS089641 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LATHIA, JUSTIN D. · 2015 to 2019
$1.7M
DEFINING RISK FACTORS FOR NF1-OPTIC GLIOMAR01CA214146 · NCI · WASHINGTON UNIVERSITY · PI GUTMANN, DAVID H · 2016 to 2020
$1.7M
Tissue Factor as a Key Determinant of IDH1 Mutant versus IDH1 Wild-type Glioma Thrombosis and MalignancyR01NS102669 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HORBINSKI, CRAIG MICHAEL · 2017 to 2021
$1.7M
Deciphering MDSC function for GBM targetingR01NS109742 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI LATHIA, JUSTIN D., VOGELBAUM, MICHAEL A. · 2019 to 2023
$1.7M
Interaction between Tissue Factor, Junctional Adhesion Molecule-A, and Integrin B1 to drive self-renewal in glioblastomaR01NS117104 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI HORBINSKI, CRAIG MICHAEL, LATHIA, JUSTIN D. · 2020 to 2024
$1.5M
NCI NIH HHS R01 CA214146NHLBI NIH HHS R01 HL119374NIGMS NIH HHS T32 GM007250NINDS NIH HHS R01 NS083629NINDS NIH HHS R01 NS089641NINDS NIH HHS R01 NS102669NINDS NIH HHS R01 NS109742NINDS NIH HHS R01 NS117104
6 · The paper itself

Abstract

Tight junction (TJ) proteins are essential for mediating interactions between adjacent cells and coordinating cellular and organ responses. Initial investigations into TJ proteins and junctional adhesion molecules (JAM) in cancer suggested a tumor-suppressive role where decreased expression led to increased metastasis. However, recent studies of the JAM family members JAM-A and JAM-C have expanded the roles of these proteins to include protumorigenic functions, including inhibition of apoptosis and promotion of proliferation, cancer stem cell biology, and epithelial-to-mesenchymal transition. JAM function by interacting with other proteins through three distinct molecular mechanisms: direct cell-cell interaction on adjacent cells, stabilization of adjacent cell surface receptors on the same cell, and interactions between JAM and cell surface receptors expressed on adjacent cells. Collectively, these diverse interactions contribute to both the pro- and antitumorigenic functions of JAM. In this review, we discuss these context-dependent functions of JAM in a variety of cancers and highlight key areas that remain poorly understood, including their potentially diverse intracellular signaling networks, their roles in the tumor microenvironment, and the consequences of posttranslational modifications on their function. These studies have implications in furthering our understanding of JAM in cancer and provide a paradigm for exploring additional roles of TJ proteins.

Indexed as

Disease ProgressionApoptosisBreast NeoplasmsCell AdhesionCell CommunicationCell MovementCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleHumansJunctional Adhesion Molecule AJunctional Adhesion Molecule CJunctional Adhesion MoleculesNeoplasm InvasivenessNeoplasm MetastasisNeoplasmsERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesJunctional Adhesion Molecule AJunctional Adhesion Molecule CJunctional Adhesion MoleculesTumor Suppressor Proteins

Identifiers

PMID32816855
PMCPMC7669553
OpenAlexW3049205015

What OpenQuestion holds

Textmetadata
LicenceTDM
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.