Mucin 21 is a key molecule involved in the incohesive growth pattern in lung adenocarcinoma.


Journal

Cancer science
ISSN: 1349-7006
Titre abrégé: Cancer Sci
Pays: England
ID NLM: 101168776

Informations de publication

Date de publication:
Sep 2019
Historique:
received: 03 12 2018
revised: 25 06 2019
accepted: 07 07 2019
pubmed: 14 7 2019
medline: 1 10 2019
entrez: 14 7 2019
Statut: ppublish

Résumé

Decreased cell adhesion has been reported as a significant negative prognostic factor of lung cancer. However, the molecular mechanisms responsible for the cell incohesiveness in lung cancer have not yet been elucidated in detail. We herein describe a rare histological variant of lung adenocarcinoma consisting almost entirely of individual cancer cells spreading in alveolar spaces in an incohesive pattern. A whole exome analysis of this case showed no genomic abnormalities in CDH1 or other genes encoding cell adhesion molecules. However, whole mRNA sequencing revealed that this case had an extremely high expression level of mucin 21 (MUC21), a mucin molecule that was previously shown to inhibit cell-cell and cell-matrix adhesion. The strong membranous expression of MUC21 was found on cancer cells using mAbs recognizing different O-glycosylated forms of MUC21. An immunohistochemical analysis of an unselected series of lung adenocarcinoma confirmed that the strong membranous expression of MUC21 correlated with incohesiveness. Thus, MUC21 could be a promising biomarker with potential diagnostic and therapeutic applications for lung adenocarcinoma showing cell incohesiveness.

Identifiants

pubmed: 31301084
doi: 10.1111/cas.14129
pmc: PMC6726699
doi:

Substances chimiques

Antigens, CD 0
CDH1 protein, human 0
Cadherins 0
MUC21 protein, human 0
Membrane Glycoproteins 0
Mucins 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

3006-3011

Informations de copyright

© 2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.

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Auteurs

Taichiro Yoshimoto (T)

Department of Integrative Pathology, Jichi Medical University, Japan.

Daisuke Matsubara (D)

Department of Integrative Pathology, Jichi Medical University, Japan.

Manabu Soda (M)

Department of Cellular Signaling, The University of Tokyo, Japan.

Toshihide Ueno (T)

Department of Cellular Signaling, The University of Tokyo, Japan.
Division of Cellular Signaling, National Cancer Center Research Institute, Japan.

Yusuke Amano (Y)

Department of Integrative Pathology, Jichi Medical University, Japan.

Atsushi Kihara (A)

Department of Integrative Pathology, Jichi Medical University, Japan.

Takashi Sakatani (T)

Department of Diagnostic Pathology, Nippon Medical School Hospital, Japan.

Tomoyuki Nakano (T)

Department of Thoracic Surgery, Jichi Medical University, Japan.

Tomoki Shibano (T)

Department of Thoracic Surgery, Jichi Medical University, Japan.

Shunsuke Endo (S)

Department of Thoracic Surgery, Jichi Medical University, Japan.

Koichi Hagiwara (K)

Division of Pulmonary Medicine, Department of Internal Medicine, Jichi Medical University, Japan.

Masashi Fukayama (M)

Human Pathology, Graduate School of Medicine, The University of Tokyo, Japan.

Kaori Denda-Nagai (K)

Division of Glycobiologics, Intractable Disease Research Center, Juntendo University, Japan.

Tatsuro Irimura (T)

Division of Glycobiologics, Intractable Disease Research Center, Juntendo University, Japan.

Hiroyuki Mano (H)

Department of Cellular Signaling, The University of Tokyo, Japan.
Division of Cellular Signaling, National Cancer Center Research Institute, Japan.

Toshiro Niki (T)

Department of Integrative Pathology, Jichi Medical University, Japan.

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Classifications MeSH