YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation

Ha, Bin; Lee, Eun Byul; Cui, Jun; Kim, Yosup

doi:10.1016/J.BBRC.2015.01.114

Title: YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation

Full Record
Other Related Research

Abstract

The Y-box binding protein-1 (YB-1) is a transcription/translation regulatory protein, and the expression thereof is associated with cancer aggressiveness. In the present study, we explored the regulatory effects of YB-1 during the transforming growth factor-β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) in lung adenocarcinoma cells. Downregulation of YB-1 increased E-cadherin promoter activity, and upregulation of YB-1 decreased promoter activity, suggesting that the YB-1 level may be correlated with the EMT. TGF-β1 induced YB-1 expression, and TGF-β1 translocated cytosolic YB-1 into the nucleus. YB-1 overexpression promoted TGF-β1-induced downregulation of epithelial markers, upregulation of mesenchymal markers, and cell migration. Moreover, YB-1 overexpression enhanced the expression of E-cadherin transcriptional repressors via TGF-β1-induced Akt activation. Our findings afford new insights into the role played by YB-1 in the TGF-β1 signaling pathway. - Highlights: • YB-1 regulates E-cadherin expression in A549 cells. • TGF-β1 induces upregulating and nuclear localization of YB-1. • YB-1 overexpression accelerates TGF-β1-induced EMT and cell migration. • YB-1 regulates Snail and Slug expression via Akt activation.

Authors:

Ha, Bin; Lee, Eun Byul; Cui, Jun; Kim, Yosup ^[1]

Department of Molecular Medicine, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-799 (Korea, Republic of)

Publication Date:: Fri Mar 06 00:00:00 EST 2015

OSTI Identifier:: 22458519

Resource Type:: Journal Article

Journal Name:: Biochemical and Biophysical Research Communications

Additional Journal Information:: Journal Volume: 458; Journal Issue: 2; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X

Country of Publication:: United States

Language:: English

Subject:: 60 APPLIED LIFE SCIENCES; CARCINOMAS; CELL NUCLEI; GROWTH FACTORS; LUNGS; PROMOTERS; SIGNALS; SNAILS; TRANSCRIPTION

Citation Formats


                    Ha, Bin, Lee, Eun Byul, Cui, Jun, Kim, Yosup, Jang, Ho Hee, E-mail: hhjang@gachon.ac.kr, and Gachon Medical Research Institute, Gil Medical Center, Gachon University, Incheon. YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation.  United States: N. p., 2015. 
        Web.  doi:10.1016/J.BBRC.2015.01.114.

Copy to clipboard


                    Ha, Bin, Lee, Eun Byul, Cui, Jun, Kim, Yosup, Jang, Ho Hee, E-mail: hhjang@gachon.ac.kr, & Gachon Medical Research Institute, Gil Medical Center, Gachon University, Incheon. YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation.  United States.  https://doi.org/10.1016/J.BBRC.2015.01.114

Copy to clipboard


                    Ha, Bin, Lee, Eun Byul, Cui, Jun, Kim, Yosup, Jang, Ho Hee, E-mail: hhjang@gachon.ac.kr, and Gachon Medical Research Institute, Gil Medical Center, Gachon University, Incheon. 2015.  
        "YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation".  United States.  https://doi.org/10.1016/J.BBRC.2015.01.114.

Copy to clipboard


                    
@article{osti_22458519,

  title        = {YB-1 overexpression promotes a TGF-β1-induced epithelial–mesenchymal transition via Akt activation},

  author       = {Ha, Bin and Lee, Eun Byul and Cui, Jun and Kim, Yosup and Jang, Ho Hee, E-mail: hhjang@gachon.ac.kr and Gachon Medical Research Institute, Gil Medical Center, Gachon University, Incheon},

  abstractNote = {The Y-box binding protein-1 (YB-1) is a transcription/translation regulatory protein, and the expression thereof is associated with cancer aggressiveness. In the present study, we explored the regulatory effects of YB-1 during the transforming growth factor-β1 (TGF-β1)-induced epithelial-to-mesenchymal transition (EMT) in lung adenocarcinoma cells. Downregulation of YB-1 increased E-cadherin promoter activity, and upregulation of YB-1 decreased promoter activity, suggesting that the YB-1 level may be correlated with the EMT. TGF-β1 induced YB-1 expression, and TGF-β1 translocated cytosolic YB-1 into the nucleus. YB-1 overexpression promoted TGF-β1-induced downregulation of epithelial markers, upregulation of mesenchymal markers, and cell migration. Moreover, YB-1 overexpression enhanced the expression of E-cadherin transcriptional repressors via TGF-β1-induced Akt activation. Our findings afford new insights into the role played by YB-1 in the TGF-β1 signaling pathway. - Highlights: • YB-1 regulates E-cadherin expression in A549 cells. • TGF-β1 induces upregulating and nuclear localization of YB-1. • YB-1 overexpression accelerates TGF-β1-induced EMT and cell migration. • YB-1 regulates Snail and Slug expression via Akt activation.},

  doi          = {10.1016/J.BBRC.2015.01.114},

  url          = {https://www.osti.gov/biblio/22458519},
  journal      = {Biochemical and Biophysical Research Communications},

  issn         = {0006-291X},

  number       = 2,

  volume       = 458,

  place        = {United States},

  year         = {Fri Mar 06 00:00:00 EST 2015},

  month        = {Fri Mar 06 00:00:00 EST 2015}

}

Copy to clipboard

Journal Article:

https://doi.org/10.1016/J.BBRC.2015.01.114

Other availability

Find in Google Scholar

Search WorldCat to find libraries that may hold this journal

Save / Share:

Export Metadata

Save to My Library

Similar records in OSTI.GOV collections:

Celastrol inhibits TGF-β1-induced epithelial–mesenchymal transition by inhibiting Snail and regulating E-cadherin expression

Journal Article Kang, Hyereen; Lee, Minjae; Jang, Sung-Wuk - Biochemical and Biophysical Research Communications

Highlights: •We investigated the effects of celastrol on TGF-β1-induced EMT in epithelial cells. •Celastrol regulates TGF-β1-induced morphological changes and E-cadherin expression. •Celastrol inhibits TGF-β1-induced Snail expression. •Celastrol strongly suppresses TGF-β1-induced invasion in MDCK and A549 cells. -- Abstract: The epithelial–mesenchymal transition (EMT) is a pivotal event in the invasive and metastatic potentials of cancer progression. Celastrol inhibits the proliferation of a variety of tumor cells including leukemia, glioma, prostate, and breast cancer; however, the possible role of celastrol in the EMT is unclear. We investigated the effect of celastrol on the EMT. Transforming growth factor-beta 1 (TGF-β1) induced EMT-like morphologicmore »« less
https://doi.org/10.1016/J.BBRC.2013.06.113
MicroRNA-29b regulates TGF-β1-mediated epithelial–mesenchymal transition of retinal pigment epithelial cells by targeting AKT2

Journal Article Li, Min; Li, Hui; Liu, Xiaoqiang; ... - Experimental Cell Research

The role of microRNA (miRNA) in proliferative vitreoretinopathy (PVR) progression has not been studied extensively, especially in retinal pigment epithelial–mesenchymal transition (EMT) which is the main reason for formation of PVR. In this study, we first investigated the miRNA expression profile in transforming growth factor beta 1 (TGF-β1) mediated EMT of ARPE-19 cells. Among the five changed miRNAs, miR-29b showed the most significant downregulation. Enhanced expression of miR-29b could reverse TGF-β1 induced EMT through targeting Akt2. Akt2 downregulation could inhibit TGF-β1-induced EMT. Furthermore, inhibition of miR-29b in ARPE-19 cells directly triggered EMT process, which characterized by the phenotypic transition andmore »« less
https://doi.org/10.1016/J.YEXCR.2014.09.026
Protective effect of Ac-SDKP on alveolar epithelial cells through inhibition of EMT via TGF-β1/ROCK1 pathway in silicosis in rat

Journal Article Deng, Haijing; Xu, Hong; Zhang, Xianghong; ... - Toxicology and Applied Pharmacology

The epithelial–mesenchymal transition (EMT) is a critical stage during the development of silicosis fibrosis. In the current study, we hypothesized that the anti-fibrotic tetrapeptide, N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) may exert its anti-fibrotic effects via activation of the TGF-β1/ROCK1 pathway, leading to inhibition of EMT. To address this hypothesis, we first examined the effect of Ac-SDKP upon EMT using an in vivo rat silicosis model, as well as in an in vitro model of TGF-β1-induced EMT. Confocal laser scanning microscopy was used to examine colocalization of surfactant protein A (SP-A), fibroblast specific protein-1 (FSP-1) and α-smooth muscle actin (α-SMA) in vivo. Western blotmore »« less
https://doi.org/10.1016/J.TAAP.2016.01.010
INPP4B reverses docetaxel resistance and epithelial-to-mesenchymal transition via the PI3K/Akt signaling pathway in prostate cancer

Journal Article Chen, Haiwen; Li, Hongliang; Chen, Qi - Biochemical and Biophysical Research Communications

Docetaxel efficiency in the therapy of prostate cancer (PCa) patients is limited due to the development of chemoresistance. Recent studies have implied a role of INPP4B in tumor chemoresistance, while the effects of INPP4B on docetaxel resistance in PCa have not been elucidated. In the present study, the docetaxel-resistant human PCa cell lines PC3-DR and DU-145-DR were established from the parental cell lines PC3 and DU-145, and the expression and role of INPP4B in docetaxel-resistant PCa cells were investigated. The results demonstrated that INPP4B expression was significantly downregulated in docetaxel-resistant cells. Overexpression of INPP4B increased the sensitivity to docetaxel andmore »« less
https://doi.org/10.1016/J.BBRC.2016.06.073
Epigenetic activation of SIN1 promotes NSCLC cell proliferation and metastasis by affecting the epithelial–mesenchymal transition

Journal Article Hu, Zhongwu; Wang, Yaqin; Wang, Yuemei; ... - Biochemical and Biophysical Research Communications

Stress-activated protein kinase (SAPK) interacting protein 1 (SIN1) is an essential component of mTORC2. Previous studies have shown that SIN1 is a key regulator of Akt pathway which plays an important role in various pathological conditions including cancer. While its effects and mechanisms on the progression of NSCLC remain unknown. In this study, we report that SIN1 is able to promote the growth and migration of NSCLC cells both in vitro and in vivo. Overexpression of SIN1 promoted A549 and H1299 cells proliferation by both MTT and colony formation assays. Consistently, knockdown of SIN1 inhibited the proliferation of these cells. In transwell assay,more »« less
https://doi.org/10.1016/J.BBRC.2016.12.089

Similar Records