Chen, Z., Wang, Y., Liu, W., Zhao, G., Lee, S., Balogh, A., Zou, Y., Guo, Y., Zhang, Z., Gu, W., Li, C., Tigyi, G., & Yue, J. (2014). Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells. PLoS ONE, 9(8), Article e105331. https://doi.org/10.1371/journal.pone.0105331
Chen, Zixuan ; Wang, Yinan ; Liu, Wen et al. / Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells. In: PLoS ONE. 2014 ; Vol. 9, No. 8.
@article{233a4b80708549c9a81bec29304b34d0,
title = "Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells",
abstract = "Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Kr{\"u}ppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.",
author = "Zixuan Chen and Yinan Wang and Wen Liu and Guannan Zhao and Suechin Lee and Andrea Balogh and Yanan Zou and Yuqi Guo and Zhan Zhang and Weiwang Gu and Chengyao Li and Gabor Tigyi and Junming Yue",
year = "2014",
month = aug,
day = "19",
doi = "10.1371/journal.pone.0105331",
language = "English",
volume = "9",
journal = "PLoS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "8",
}
Chen, Z, Wang, Y, Liu, W, Zhao, G, Lee, S, Balogh, A, Zou, Y, Guo, Y, Zhang, Z, Gu, W, Li, C, Tigyi, G & Yue, J 2014, 'Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells', PLoS ONE, vol. 9, no. 8, e105331. https://doi.org/10.1371/journal.pone.0105331
Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells. /
Chen, Zixuan; Wang, Yinan; Liu, Wen et al.
In:
PLoS ONE, Vol. 9, No. 8, e105331, 19.08.2014.
Research output: Contribution to journal › Article › peer-review
TY - JOUR
T1 - Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells
AU - Chen, Zixuan
AU - Wang, Yinan
AU - Liu, Wen
AU - Zhao, Guannan
AU - Lee, Suechin
AU - Balogh, Andrea
AU - Zou, Yanan
AU - Guo, Yuqi
AU - Zhang, Zhan
AU - Gu, Weiwang
AU - Li, Chengyao
AU - Tigyi, Gabor
AU - Yue, Junming
PY - 2014/8/19
Y1 - 2014/8/19
N2 - Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.
AB - Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.
UR - http://www.scopus.com/inward/record.url?scp=84929113339&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0105331
DO - 10.1371/journal.pone.0105331
M3 - Article
C2 - 25137052
AN - SCOPUS:84929113339
SN - 1932-6203
VL - 9
JO - PLoS ONE
JF - PLoS ONE
IS - 8
M1 - e105331
ER -
Chen Z, Wang Y, Liu W, Zhao G, Lee S, Balogh A et al. Doxycycline inducible Kruppel-like factor 4 lentiviral vector mediates mesenchymal to epithelial transition in ovarian cancer cells. PLoS ONE. 2014 Aug 19;9(8):e105331. doi: 10.1371/journal.pone.0105331
