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14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway
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| Veröffentlicht in: | OncoTarget 7(2016), 34, Seite 55191-55210 |
|---|---|
| Personen und Körperschaften: | , |
| Titel: | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway/ Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang |
| Format: | E-Book-Kapitel |
| Sprache: | Englisch |
| veröffentlicht: |
8 July 2016
|
| Gesamtaufnahme: |
: OncoTarget, 7(2016), 34, Seite 55191-55210
, volume:7 |
| Quelle: | Verbunddaten SWB Lizenzfreie Online-Ressourcen |
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| 246 | 3 | 3 | |a 14-3-3 [zeta] and aPKC- [iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3 beta/snail signaling pathway |
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| 520 | |a Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3ζ and atypical protein kinase C-ι (aPKC-ι) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3ζ and aPKC-ι co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3β)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3ζ and aPKC-ι was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3ζ and aPKC-ι expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3ζ and aPKC-ι. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3ζ and aPKC-ι regulated each other. In addition, 14-3-3ζ and aPKC-ι pretreatment by si-RNA inhibit the phosphorylated GSK-3β and Snail expression during EMT. Meanwhile, silence of 14-3-3ζ or aPKC-ι suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3ζ and aPKC-ι synergistically facilitate EMT of CCA via GSK-3β/Snail signalling pathway, and may be potential therapeutic target for CCA. | ||
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| contents | Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3ζ and atypical protein kinase C-ι (aPKC-ι) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3ζ and aPKC-ι co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3β)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3ζ and aPKC-ι was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3ζ and aPKC-ι expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3ζ and aPKC-ι. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3ζ and aPKC-ι regulated each other. In addition, 14-3-3ζ and aPKC-ι pretreatment by si-RNA inhibit the phosphorylated GSK-3β and Snail expression during EMT. Meanwhile, silence of 14-3-3ζ or aPKC-ι suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3ζ and aPKC-ι synergistically facilitate EMT of CCA via GSK-3β/Snail signalling pathway, and may be potential therapeutic target for CCA. |
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| spelling | Yang, Yan VerfasserIn (DE-588)1154451593 (DE-627)1015741959 (DE-576)500999945 aut, 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang, ζ ι β 14-3-3ζ and aPKC-ι, 14-3-3 [zeta] and aPKC- [iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3 beta/snail signaling pathway, 8 July 2016, 20, Text txt rdacontent, Computermedien c rdamedia, Online-Ressource cr rdacarrier, Gesehen am 13.03.2018, Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3ζ and atypical protein kinase C-ι (aPKC-ι) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3ζ and aPKC-ι co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3β)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3ζ and aPKC-ι was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3ζ and aPKC-ι expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3ζ and aPKC-ι. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3ζ and aPKC-ι regulated each other. In addition, 14-3-3ζ and aPKC-ι pretreatment by si-RNA inhibit the phosphorylated GSK-3β and Snail expression during EMT. Meanwhile, silence of 14-3-3ζ or aPKC-ι suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3ζ and aPKC-ι synergistically facilitate EMT of CCA via GSK-3β/Snail signalling pathway, and may be potential therapeutic target for CCA., Schemmer, Peter 1967- VerfasserIn (DE-588)1022604244 (DE-627)717006794 (DE-576)365668230 aut, Enthalten in OncoTarget [S.l.] : Impact Journals LLC, 2010 7(2016), 34, Seite 55191-55210 Online-Ressource (DE-627)63035975X (DE-600)2560162-3 (DE-576)325343764 1949-2553 nnns, volume:7 year:2016 number:34 pages:55191-55210 extent:20, http://dx.doi.org/10.18632/oncotarget.10483 Verlag Resolving-System kostenfrei Volltext, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5342411/ Verlag kostenfrei Volltext, http://dx.doi.org/10.18632/oncotarget.10483 LFER, LFER 2018-04-10T00:00:00Z |
| spellingShingle | Yang, Yan, Schemmer, Peter, 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway, Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3ζ and atypical protein kinase C-ι (aPKC-ι) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3ζ and aPKC-ι co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3β)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3ζ and aPKC-ι was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3ζ and aPKC-ι expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3ζ and aPKC-ι. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3ζ and aPKC-ι regulated each other. In addition, 14-3-3ζ and aPKC-ι pretreatment by si-RNA inhibit the phosphorylated GSK-3β and Snail expression during EMT. Meanwhile, silence of 14-3-3ζ or aPKC-ι suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3ζ and aPKC-ι synergistically facilitate EMT of CCA via GSK-3β/Snail signalling pathway, and may be potential therapeutic target for CCA. |
| swb_id_str | 501000097 |
| title | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway |
| title_alt | ζ ι β 14-3-3ζ and aPKC-ι, 14-3-3 [zeta] and aPKC- [iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3 beta/snail signaling pathway |
| title_auth | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway |
| title_full | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang |
| title_fullStr | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang |
| title_full_unstemmed | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang |
| title_in_hierarchy | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway / Yan Yang, Yan Liu, Jun-chuang He, Jian-ming Wang, Peter Schemmer, Chao-qun Ma, Ya-wei Qian, Wei Yao, Jian Zhang, Wei-peng Qi, Yang Fu, Wei Feng, Tao Yang, |
| title_short | 14-3-3[zeta] and aPKC-[iota] synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3β/snail signaling pathway |
| title_sort | 14 3 3 zeta and apkc iota synergistically facilitate epithelial mesenchymal transition of cholangiocarcinoma via gsk 3β snail signaling pathway |
| url | http://dx.doi.org/10.18632/oncotarget.10483, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5342411/ |