ID 13696
File
Authors
Matsushige, Takahiro Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University
Sakabe, Tomohiko Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University Researchers DB KAKEN
Umekita, Yoshihisa Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University Researchers DB KAKEN
Keywords
lung adenocarcinoma
maspin
Abstract
Background: Mammary serine protease inhibitor (maspin) is well known as a tumor suppressor gene in several types of cancers and its nuclear localization is essential for its tumor-suppressive function. We previously reported that the cytoplasmic-only localization of maspin is significantly correlated with unfavorable prognosis in patients with lung adenocarcinoma (LUAD). To clarify whether maspin in LUAD acts as a tumor promoter or suppressor, we examined the subcellular localization-dependent biological functions of maspin in human LUAD cell lines. Methods: The expression levels and subcellular localization of maspin were investigated by performing immunoblotting and immunofluorescence in human LUAD cell lines (PC-9, A549, NCI-H23, RERF-LCKJ) and human bronchial epithelial cell line (BEAS-2B). We then established stable cell lines overexpressing maspin (A549-maspin and RERF-LC-KJ-maspin) and investigated their subcellular localization. Cell invasion assays of these cell lines were performed to examine their invasiveness. Moreover, the mRNA expression levels between epithelial cell markers (E-cadherin) and mesenchymal cell markers (N-cadherin and vimentin) were compared. Results: The expression of maspin in PC-9 cells was comparable to that in BEAS-2B cells, whereas its expression in A549, NCI-H23, and RERF-LC-KJ cells was decreased. The cell invasion capability of A549-maspin cells showing pancellular expression was significantly decreased compared with that of A549-control cells. By contrast, the cell invasion capability of RERF-LC-KJmaspin cells showing cytoplasmic-only expression was significantly increased compared with that of RERFLC-KJ-control cells. The mRNA expression levels of N-cadherin, but not E-cadherin and vimentin, in A549-maspin cells was significantly downregulated compared with that in A549-control cells. No significant differences in these markers were observed between RERFLC-KJ-maspin and RERF-LC-KJ-control cells. Conclusion: The invasive capability of LUAD cells is regulated by the intracellular localization of maspin. Clarification of the molecular mechanism underlying the subcellular localization-dependent function of maspin will promote a deeper understanding of LUAD development and progression.
Publisher
Tottori University Medical Press
Content Type
Journal Article
Link
ISSN
05135710
EISSN
13468049
NCID
AA00892882
Journal Title
Yonago Acta Medica
Current Journal Title
Yonago Acta Medica
Volume
65
Issue
1
Start Page
44
End Page
52
Published Date
2022-02-22
Publisher-DOI
Text Version
Publisher
Rights
(C) 2022 Tottori University Medical Press.
Citation
Yonago Acta Medica. 2022, 65(1), 44-52. doi10.33160/yam.2022.02.006
Department
Faculty of Medicine/Graduate School of Medical Sciences/University Hospital
Language
English