SATB 2 suppresses the progression of colorectal cancer cells via inactivation of MEK 5/ERK 5 signaling

Journal article


Mansour, M.A., Hyodo, T., Ito, S., Kurita, K., Kokuryo, T., Uehara, K., Nagino, M., Takahashi, M., Hamaguchi, M. and Senga, T. (2015). SATB 2 suppresses the progression of colorectal cancer cells via inactivation of MEK 5/ERK 5 signaling. The FEBS journal. 282 (8), pp. 1394-1405. https://doi.org/10.1111/febs.13227
AuthorsMansour, M.A., Hyodo, T., Ito, S., Kurita, K., Kokuryo, T., Uehara, K., Nagino, M., Takahashi, M., Hamaguchi, M. and Senga, T.
Abstract

Special AT ‐rich sequence binding protein 2 (SATB 2) is an evolutionarily conserved transcription factor that has multiple roles in neuronal development, osteoblast differentiation, and craniofacial patterning. SATB 2 binds to the nuclear matrix attachment region, and regulates the expression of diverse sets of genes by altering chromatin structure. Recent studies have reported that high expression of SATB 2 is associated with favorable prognosis in colorectal and laryngeal cancer; however, it remains uncertain whether SATB 2 has tumor‐suppressive functions in cancer cells. In this study, we examined the effects of SATB 2 expression on the malignant characteristics of colorectal cancer cells. Expression of SATB 2 repressed the proliferation of cancer cells in vitro and in vivo , and also suppressed their migration and invasion. Extracellular signal‐regulated kinase 5 (ERK 5) is a mitogen‐activated protein kinase that is associated with an aggressive phenotype in various types of cancer. SATB 2 expression reduced the activity of ERK 5, and constitutive activation of ERK 5 restored the proliferation, anchorage‐independent growth, migration and invasion of SATB 2‐expressing cells. Our results demonstrate the existence of a novel regulatory mechanism of SATB 2‐mediated tumor suppression via ERK 5 inactivation.

Year2015
JournalThe FEBS journal
Journal citation282 (8), pp. 1394-1405
PublisherWiley
Digital Object Identifier (DOI)https://doi.org/10.1111/febs.13227
Publication dates
Online07 Feb 2015
Publication process dates
Accepted04 Feb 2015
Deposited10 Aug 2020
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