@article{bassey-archibong_kaiso_2016,
	title = {Kaiso depletion attenuates transforming growth factor-β signaling and metastatic activity of triple-negative breast cancer cells},
	volume = {5},
	issn = {2157-9024},
	url = {http://www.ncbi.nlm.nih.gov/pubmed/26999717 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4815049 http://www.nature.com/articles/oncsis201617},
	doi = {10.1038/oncsis.2016.17},
	abstract = {Triple-negative breast cancers (TNBCs) represent a subset of breast tumors that are highly aggressive and metastatic, and are responsible for a disproportionate number of breast cancer-related deaths. Several studies have postulated a role for the epithelial-to-mesenchymal transition (EMT) program in the increased aggressiveness and metastatic propensity of TNBCs. Although EMT is essential for early vertebrate development and wound healing, it is frequently co-opted by cancer cells during tumorigenesis. One prominent signaling pathway involved in EMT is the transforming growth factor-β (TGFβ) pathway. In this study, we report that the novel POZ-ZF transcription factor Kaiso is highly expressed in TNBCs and correlates with a shorter metastasis-free survival. Notably, Kaiso expression is induced by the TGFβ pathway and silencing Kaiso expression in the highly invasive breast cancer cell lines, MDA-MB-231 (hereafter MDA-231) and Hs578T, attenuated the expression of several EMT-associated proteins (Vimentin, Slug and ZEB1), abrogated TGFβ signaling and TGFβ-dependent EMT. Moreover, Kaiso depletion attenuated the metastasis of TNBC cells (MDA-231 and Hs578T) in a mouse model. Although high Kaiso and high TGFβR1 expression is associated with poor overall survival in breast cancer patients, overexpression of a kinase-active TGFβR1 in the Kaiso-depleted cells was insufficient to restore the metastatic potential of these cells, suggesting that Kaiso is a key downstream component of TGFβ-mediated pro-metastatic responses. Collectively, these findings suggest a critical role for Kaiso in TGFβ signaling and the metastasis of TNBCs.},
	number = {3},
	journal = {Oncogenesis},
	author = {Bassey-Archibong, B I and Kwiecien, J M and Milosavljevic, S B and Hallett, R M and Rayner, L G A and Erb, M J and Crawford-Brown, C J and Stephenson, K B and Bédard, P-A and Hassell, J A and Daniel, J M},
	month = mar,
	year = {2016},
	pmid = {26999717},
	pages = {e208--e208},
}

{"_id":"8Ac6pY4o7ELJ9PBpg","bibbaseid":"basseyarchibong-kwiecien-milosavljevic-hallett-rayner-erb-crawfordbrown-stephenson-etal-kaisodepletionattenuatestransforminggrowthfactorsignalingandmetastaticactivityoftriplenegativebreastcancercells-2016","authorIDs":[],"author_short":["Bassey-Archibong, B I","Kwiecien, J M","Milosavljevic, S B","Hallett, R M","Rayner, L G A","Erb, M J","Crawford-Brown, C J","Stephenson, K B","Bédard, P.","Hassell, J A","Daniel, J M"],"bibdata":{"bibtype":"article","type":"article","title":"Kaiso depletion attenuates transforming growth factor-β signaling and metastatic activity of triple-negative breast cancer cells","volume":"5","issn":"2157-9024","url":"http://www.ncbi.nlm.nih.gov/pubmed/26999717 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4815049 http://www.nature.com/articles/oncsis201617","doi":"10.1038/oncsis.2016.17","abstract":"Triple-negative breast cancers (TNBCs) represent a subset of breast tumors that are highly aggressive and metastatic, and are responsible for a disproportionate number of breast cancer-related deaths. Several studies have postulated a role for the epithelial-to-mesenchymal transition (EMT) program in the increased aggressiveness and metastatic propensity of TNBCs. Although EMT is essential for early vertebrate development and wound healing, it is frequently co-opted by cancer cells during tumorigenesis. One prominent signaling pathway involved in EMT is the transforming growth factor-β (TGFβ) pathway. In this study, we report that the novel POZ-ZF transcription factor Kaiso is highly expressed in TNBCs and correlates with a shorter metastasis-free survival. Notably, Kaiso expression is induced by the TGFβ pathway and silencing Kaiso expression in the highly invasive breast cancer cell lines, MDA-MB-231 (hereafter MDA-231) and Hs578T, attenuated the expression of several EMT-associated proteins (Vimentin, Slug and ZEB1), abrogated TGFβ signaling and TGFβ-dependent EMT. Moreover, Kaiso depletion attenuated the metastasis of TNBC cells (MDA-231 and Hs578T) in a mouse model. Although high Kaiso and high TGFβR1 expression is associated with poor overall survival in breast cancer patients, overexpression of a kinase-active TGFβR1 in the Kaiso-depleted cells was insufficient to restore the metastatic potential of these cells, suggesting that Kaiso is a key downstream component of TGFβ-mediated pro-metastatic responses. Collectively, these findings suggest a critical role for Kaiso in TGFβ signaling and the metastasis of TNBCs.","number":"3","journal":"Oncogenesis","author":[{"propositions":[],"lastnames":["Bassey-Archibong"],"firstnames":["B","I"],"suffixes":[]},{"propositions":[],"lastnames":["Kwiecien"],"firstnames":["J","M"],"suffixes":[]},{"propositions":[],"lastnames":["Milosavljevic"],"firstnames":["S","B"],"suffixes":[]},{"propositions":[],"lastnames":["Hallett"],"firstnames":["R","M"],"suffixes":[]},{"propositions":[],"lastnames":["Rayner"],"firstnames":["L","G","A"],"suffixes":[]},{"propositions":[],"lastnames":["Erb"],"firstnames":["M","J"],"suffixes":[]},{"propositions":[],"lastnames":["Crawford-Brown"],"firstnames":["C","J"],"suffixes":[]},{"propositions":[],"lastnames":["Stephenson"],"firstnames":["K","B"],"suffixes":[]},{"propositions":[],"lastnames":["Bédard"],"firstnames":["P-A"],"suffixes":[]},{"propositions":[],"lastnames":["Hassell"],"firstnames":["J","A"],"suffixes":[]},{"propositions":[],"lastnames":["Daniel"],"firstnames":["J","M"],"suffixes":[]}],"month":"March","year":"2016","pmid":"26999717","pages":"e208–e208","bibtex":"@article{bassey-archibong_kaiso_2016,\n\ttitle = {Kaiso depletion attenuates transforming growth factor-β signaling and metastatic activity of triple-negative breast cancer cells},\n\tvolume = {5},\n\tissn = {2157-9024},\n\turl = {http://www.ncbi.nlm.nih.gov/pubmed/26999717 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC4815049 http://www.nature.com/articles/oncsis201617},\n\tdoi = {10.1038/oncsis.2016.17},\n\tabstract = {Triple-negative breast cancers (TNBCs) represent a subset of breast tumors that are highly aggressive and metastatic, and are responsible for a disproportionate number of breast cancer-related deaths. Several studies have postulated a role for the epithelial-to-mesenchymal transition (EMT) program in the increased aggressiveness and metastatic propensity of TNBCs. Although EMT is essential for early vertebrate development and wound healing, it is frequently co-opted by cancer cells during tumorigenesis. One prominent signaling pathway involved in EMT is the transforming growth factor-β (TGFβ) pathway. In this study, we report that the novel POZ-ZF transcription factor Kaiso is highly expressed in TNBCs and correlates with a shorter metastasis-free survival. Notably, Kaiso expression is induced by the TGFβ pathway and silencing Kaiso expression in the highly invasive breast cancer cell lines, MDA-MB-231 (hereafter MDA-231) and Hs578T, attenuated the expression of several EMT-associated proteins (Vimentin, Slug and ZEB1), abrogated TGFβ signaling and TGFβ-dependent EMT. Moreover, Kaiso depletion attenuated the metastasis of TNBC cells (MDA-231 and Hs578T) in a mouse model. Although high Kaiso and high TGFβR1 expression is associated with poor overall survival in breast cancer patients, overexpression of a kinase-active TGFβR1 in the Kaiso-depleted cells was insufficient to restore the metastatic potential of these cells, suggesting that Kaiso is a key downstream component of TGFβ-mediated pro-metastatic responses. 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