ArticleInternational journal of clinical oncology2015
CXCR4 promotes GSK3β expression in pancreatic cancer cells via the Akt pathway.
Article in International journal of clinical oncology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- G-CSF promotes H3K27ac-modified KLF5 to activate CXCR4 expression and drive colon cancer growth and metastasis.European journal of medical research · 2026Article
- Stem cell-like circulating tumor cells identified by Pep@MNP and their clinical significance in pancreatic cancer metastasis.Frontiers in oncology · 2024Article
- Alkannin Induces G2/M-Phase Arrest, Apoptosis, and Inhibition of Invasion by Targeting GSK3β in Esophageal Squamous Cell Carcinoma.Drug design, development and therapy · 2024Article
- Glycogen synthase kinase 3β: the nexus of chemoresistance, invasive capacity, and cancer stemness in pancreatic cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- The upregulation of stromal antigen 3 expression suppresses the phenotypic hallmarks of hepatocellular carcinoma through the Smad3-CDK4/CDK6-cyclin D1 and CXCR4/RhoA pathways.BMC gastroenterology · 2022Article
- Review
- Molecular targets for the treatment of pancreatic cancer: Clinical and experimental studies.World journal of gastroenterology · 2016Review
- Plumbagin induces G2/M arrest, apoptosis, and autophagy via p38 MAPK- and PI3K/Akt/mTOR-mediated pathways in human tongue squamous cell carcinoma cells.Drug design, development and therapy · 2015Article
- Genetic factors affecting patient responses to pancreatic cancer treatment.Annals of gastroenterologyReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCXCR4 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.
methodsPANC-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.
resultsOverexpression 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.
conclusionsCXCR4 promotes GSK3β expression via the Akt cell signaling pathway in pancreatic cancer cells.
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