Please use this identifier to cite or link to this item: https://hdl.handle.net/11499/8928
Title: The crosstalk between p38 and Akt signaling pathways orchestrates EMT by regulating SATB2 expression in NSCLC cells
Authors: Küçüksayan, Hakan
Akça, Hakan
Keywords: Akt
epithelial–mesenchymal transition
non-small-cell lung cancer
p38
SATB2
mitogen activated protein kinase p38
phosphatidylinositol 3,4,5 trisphosphate 3 phosphatase
protein kinase B
transcription factor
transcription factor SATB2
unclassified drug
matrix attachment region binding protein
PTEN protein, human
SATB2 protein, human
Akt signaling
Article
AT rich sequence
controlled study
enzyme activation
epigenetics
epithelial mesenchymal transition
gene silencing
lung metastasis
lung non-small cell carcinoma cell line
molecular dynamics
molecular interaction
non small cell lung cancer
priority journal
protein expression
upregulation
biosynthesis
gene expression regulation
human
lung tumor
MAPK signaling
metabolism
pathology
physiology
signal transduction
tumor cell line
Western blotting
Blotting, Western
Carcinoma, Non-Small-Cell Lung
Cell Line, Tumor
Epithelial-Mesenchymal Transition
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Humans
Lung Neoplasms
MAP Kinase Signaling System
Matrix Attachment Region Binding Proteins
Proto-Oncogene Proteins c-akt
PTEN Phosphohydrolase
Receptor Cross-Talk
Signal Transduction
Transcription Factors
Publisher: SAGE Publications Ltd
Abstract: Epithelial–mesenchymal transition is a crucial event for metastasis and could be mediated by several pathways such as phosphoinositide 3-kinase/Akt, mitogen-activated protein kinases, as well as many epigenetic regulators. Special AT-rich sequence-binding protein 2 is an epigenetic regulator involved in epithelial–mesenchymal transition and osteoblastic differentiation. It has been reported that the crosstalk between several pathways is responsible for the regulation of epithelial–mesenchymal transition in cancer cells. However, crosstalks between p38 and Akt pathways involved in epithelial–mesenchymal transition are still unknown. We recently reported that there is a crosstalk between p38 and Akt pathways in non-small-cell lung carcinoma cells, and this crosstalk is associated with E-cadherin and special AT-rich sequence-binding protein 2 expressions. Therefore, we aimed to determine whether this crosstalk has a mediator role in the regulation of epithelial–mesenchymal transition in non-small-cell lung carcinoma. Our results showed that inhibition of p38 leads to the disruption of this crosstalk via decreased expression of phosphatase and tensin homolog (PTEN) and subsequently increased activation of Akt in non-small-cell lung carcinoma cells. Then, we found that p38 inhibition upregulated special AT-rich sequence-binding protein 2 expression and reversed epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. Furthermore, special AT-rich sequence-binding protein 2 knockdown abolished the effect of p38 inhibition on epithelial–mesenchymal transition in non-small-cell lung carcinoma cells. In conclusion, our results strongly indicate that the crosstalk between p38 and Akt pathways can determine special AT-rich sequence-binding protein 2 expression and epithelial character of non-small-cell lung carcinoma cells, and special AT-rich sequence-binding protein 2 is a critical epigenetic regulator for epithelial–mesenchymal transition mediated by p38 pathway in non-small-cell lung carcinoma. Our findings will contribute to illuminate the molecular mechanisms of the epithelial–mesenchymal transition process that has a critical significance for lung cancer metastasis. © 2017, © The Author(s) 2017.
URI: https://hdl.handle.net/11499/8928
https://doi.org/10.1177/1010428317706212
ISSN: 1010-4283
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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