E-Cadherin repression increases amount of cancer stem cells in human A549 lung adenocarcinoma and stimulates tumor growth

Here we show that cancer stem cells amount in human lung adenocarcinoma cell line A549 depends on E-cadherin expression. In fact, downregulation of E-cadherin expression enhanced expression of pluripotent genes (c-MYC, NESTIN, OCT3/4 and SOX2) and enriched cell population with the cells possessing t...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2016-01, Vol.15 (8), p.1084-1092
Main Authors: Farmakovskaya, M, Khromova, N, Rybko, V, Dugina, V, Kopnin, B, Kopnin, P
Format: Article
Language:English
Subjects:
A549 Cells
Adenocarcinoma - genetics
Adenocarcinoma - pathology
Adenocarcinoma of Lung
Animals
Antigens, CD
Cadherins - genetics
Cadherins - metabolism
Carcinogenesis - genetics
Carcinogenesis - pathology
Cell Count
Cell Proliferation
Cell Shape
Gene Expression Regulation, Neoplastic
Humans
Lung Neoplasms - genetics
Lung Neoplasms - pathology
Mice, Nude
Models, Biological
Neoplastic Stem Cells - metabolism
Neoplastic Stem Cells - pathology
Repressor Proteins - metabolism
RNA, Small Interfering - metabolism
Wnt Signaling Pathway - genetics
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Summary:Here we show that cancer stem cells amount in human lung adenocarcinoma cell line A549 depends on E-cadherin expression. In fact, downregulation of E-cadherin expression enhanced expression of pluripotent genes (c-MYC, NESTIN, OCT3/4 and SOX2) and enriched cell population with the cells possessing the properties of so-called 'cancer stem cells' via activation of Wnt/β-catenin signaling. Repression of E-cadherin also stimulated cell proliferation and migration in vitro, decreased cell amount essential for xenografts formation in nude mice, increased tumors vascularization and growth. On the other hand, E-cadherin upregulation caused opposite effects i.e. diminished the number of cancer stem cells, decreased xenograft vascularization and decelerated tumor growth. Therefore, agents restoring E-cadherin expression may be useful in anticancer therapy.
ISSN:1538-4101
1551-4005
DOI:10.1080/15384101.2016.1156268