フルテキストファイル
著者
Matsushige, Takahiro Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University
坂部 友彦 Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University 研究者総覧 KAKEN
梅北 善久 Department of Pathology, School of Medicine, Faculty of Medicine, Tottori University 研究者総覧 KAKEN
キーワード
lung adenocarcinoma
maspin
抄録
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.
出版者
Tottori University Medical Press
資料タイプ
学術雑誌論文
外部リンク
ISSN
05135710
EISSN
13468049
書誌ID
AA00892882
掲載誌名
Yonago Acta Medica
最新掲載誌名
Yonago Acta Medica
65
1
開始ページ
44
終了ページ
52
発行日
2022-02-22
出版者DOI
著者版フラグ
出版社版
著作権表記
(C) 2022 Tottori University Medical Press.
掲載情報
Yonago Acta Medica. 2022, 65(1), 44-52. doi10.33160/yam.2022.02.006
部局名
医学部・医学系研究科・医学部附属病院
言語
英語