Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/9495
Title: Downregulation of SATB2 is critical for induction of epithelial-to-mesenchymal transition and invasion of NSCLC cells
Authors: Küçüksayan, Hakan
Ozes, O.N.
Akça, Hakan
Keywords: EMT
Invasion
NSCLC
SATB2
Stemness
TGF-ß
Hermes antigen
octamer transcription factor 4
small interfering RNA
special at rich binding protein 2
transcription factor
transcription factor NANOG
transcription factor Slug
transcription factor Sox2
transcription factor Twist
transcription factor ZEB1
transforming growth factor beta
unclassified drug
biological marker
nerve cell adhesion molecule
STAB2 protein, human
A549 cell line
Article
cell culture
cell invasion
controlled study
down regulation
epithelial mesenchymal transition
fibroblast
gene silencing
human
human cell
morphology
non small cell lung cancer
priority journal
protein expression
upregulation
Western blotting
cancer stem cell
cell transformation
gene expression regulation
genetics
lung tumor
metabolism
pathology
tumor cell line
tumor invasion
Biomarkers
Carcinoma, Non-Small-Cell Lung
Cell Adhesion Molecules, Neuronal
Cell Line, Tumor
Cell Transformation, Neoplastic
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Gene Silencing
Humans
Lung Neoplasms
Neoplasm Invasiveness
Neoplastic Stem Cells
Publisher: Elsevier Ireland Ltd
Abstract: Objectives: The epithelial-to-mesenchymal transition (EMT) is considered as a key step in invasion of cancer cells. There are several regulator proteins responsible for induction of EMT, but underlying mechanisms are still unclear. SATB2 is an epigenetic regulator involved in osteoblastic differentiation. The role of SATB2 in EMT and invasion of NSCLC cells is unknown. Therefore, we aimed to explain roles of SATB2 with underlying molecular mechanisms in EMT and invasion of NSCLC cells. Materials and methods: We used A549 and NCI-H1650 cells as a model to evaluate the effects of SATB2 in EMT and invasion of NSCLC cells. Cell culture, western blot analysis, siRNA-mediated gene knockdown, and invasion assay were performed in this study. Results and conclusion: In this study, we investigated the regulatory role of SATB2 expression in TGF-ß-induced EMT and invasion of NSCLC cells, and found that SATB2 is downregulated in A549 cells and TGF-ß can induce EMT in these cells, however, TGF-ß can not induce EMT in SATB2 expressing cells such as H1650, PC3, II-18, Hcc78 and Hcc193. Our results demonstrated that SATB2 knockdown is sufficient to induce generation of fibroblast-like morphology, EMT and invasion of NSCLC cells by upregulating the expressions of Slug, Twist and Zeb1. Moreover, SATB2 knockdown promotes TGF-ß-induced EMT and invasion in NSCLC cells. These results strongly suggest that SATB2 prevents induction of EMT by suppressing expression of EMT-inducing transcription factors in NSCLC cells. Furthermore, SATB2 could inhibit tumour initiation by suppressing stemness marker genes such as CD44, Nanog, Oct-4A and Sox-2. Consequently, our results clearly indicate that SATB2 plays pivotal role in EMT, invasion and stemness of NSCLC cells. © 2016 Elsevier Ireland Ltd.
URI: https://hdl.handle.net/11499/9495
https://doi.org/10.1016/j.lungcan.2016.05.032
ISSN: 0169-5002
Appears in Collections:PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection
Tıp Fakültesi Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection

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