Tumour-suppression function of KLF12 through regulation of anoikis.
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Embargo End Date
ICR Authors
Authors
Godin-Heymann, N
Brabetz, S
Murillo, MM
Saponaro, M
Santos, CR
Lobley, A
East, P
Chakravarty, P
Matthews, N
Kelly, G
Jordan, S
Castellano, E
Downward, J
Brabetz, S
Murillo, MM
Saponaro, M
Santos, CR
Lobley, A
East, P
Chakravarty, P
Matthews, N
Kelly, G
Jordan, S
Castellano, E
Downward, J
Document Type
Journal Article
Date
2016-06
Date Accepted
2015-09-05
Abstract
Suppression of detachment-induced cell death, known as anoikis, is an essential step for cancer metastasis to occur. We report here that expression of KLF12, a member of the Kruppel-like family of transcription factors, is downregulated in lung cancer cell lines that have been selected to grow in the absence of cell adhesion. Knockdown of KLF12 in parental cells results in decreased apoptosis following cell detachment from matrix. KLF12 regulates anoikis by promoting the cell cycle transition through S phase and therefore cell proliferation. Reduced expression levels of KLF12 results in increased ability of lung cancer cells to form tumours in vivo and is associated with poorer survival in lung cancer patients. We therefore identify KLF12 as a novel metastasis-suppressor gene whose loss of function is associated with anoikis resistance through control of the cell cycle.
Citation
Oncogene, 2016, 35 (25), pp. 3324 - 3334
Source Title
Publisher
ISSN
0950-9232
eISSN
1476-5594
Collections
Research Team
Lung Cancer Group