caa a22 4500 605490945 CHVBK 20210128100507.0 cr unu---uuuuu 210128e20150601xx s 000 0 eng 10.1007/s10147-014-0740-0 doi (NATIONALLICENCE)springer-10.1007/s10147-014-0740-0 CXCR4 promotes GSK3β expression in pancreatic cancer cells via the Akt pathway [Elektronische Daten] [Shijie Ma, Qianjun Li, Feng Pan] Background: CXCR4 and glycogen synthase kinase-3β (GSK3β) promote proliferation and invasion of pancreatic cancer. Inhibition of CXCR4 suppresses GSK3β expression. However, the molecular mechanism by which CXCR4 contributes to human pancreatic cancer metastasis is not completely understood. In this study, therefore, we analyzed the effect of CXCR4 on GSK3β expression and its molecular mechanism. Methods: PANC-1 and SW-1990 cells were used in this study. PANC-1 and SW-1990 cell lines which stably expressed upregulated or downregulated CXCR4 were used for further study. Western blotting was employed to detected the expression of CXCR4, GSK3β and MMP-2. Cell invasion assay was used to detect the effect of the Akt pathway on CXCR4-induced GSK3β expression. Results: Overexpression of CXCR4 promoted GSK3β expression and silencing of CXCR4 suppressed GSK3β expression. Overexpression of CXCR4 activated cyclin D1 and p-Akt expression, but inhibited p21 expression. Silencing of CXCR4 had the reverse effect. CXCR4 promoted GSK3β expression and PANC-1 invasion by Akt signaling. CXCR4 upregulated GSK3β expression, at least in part, at the level of transcription. Conclusions: CXCR4 promotes GSK3β expression via the Akt cell signaling pathway in pancreatic cancer cells. Japan Society of Clinical Oncology, 2014 CXCR4 receptor nationallicence Glycogen synthase kinase 3 nationallicence Pancreatic cancer nationallicence Ma Shijie Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut Li Qianjun Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut Pan Feng Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut International Journal of Clinical Oncology Springer Japan 20/3(2015-06-01), 525-530 1341-9625 20:3<525 2015 20 10147 https://doi.org/10.1007/s10147-014-0740-0 text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s10147-014-0740-0 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ma Shijie Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut NATIONALLICENCE 700 1- Li Qianjun Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut NATIONALLICENCE 700 1- Pan Feng Department of Gastroenterology, Huai'an First People's Hospital, Nanjing Medical University, 6 Beijing Road West, 223300, Huai'an, Jiangsu, People's Republic of China aut NATIONALLICENCE 773 0- International Journal of Clinical Oncology Springer Japan 20/3(2015-06-01), 525-530 1341-9625 20:3<525 2015 20 10147