scholarly journals Signal Transducer and Activator of Transcription 3 Is Required for Hypoxia-Inducible Factor-1α RNA Expression in Both Tumor Cells and Tumor-Associated Myeloid Cells

2008 ◽  
Vol 6 (7) ◽  
pp. 1099-1105 ◽  
Author(s):  
Guilian Niu ◽  
Jon Briggs ◽  
Jiehui Deng ◽  
Yihong Ma ◽  
Heehyoung Lee ◽  
...  
PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30999 ◽  
Author(s):  
Yilu Lu ◽  
Kun Zhang ◽  
Chao Li ◽  
Youlin Yao ◽  
Dachang Tao ◽  
...  

2010 ◽  
Vol 66 (5) ◽  
pp. 899-911 ◽  
Author(s):  
Sreenivasulu Chintala ◽  
Károly Tόth ◽  
Shousong Cao ◽  
Farukh A. Durrani ◽  
Mary M. Vaughan ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Amr Allam ◽  
Marina Yakou ◽  
Lokman Pang ◽  
Matthias Ernst ◽  
Jennifer Huynh

The tumor microenvironment (TME) is composed of a heterogenous population of cells that exist alongside the extracellular matrix and soluble components. These components can shape an environment that is conducive to tumor growth and metastatic spread. It is well-established that stromal cancer-associated fibroblasts (CAFs) in the TME play a pivotal role in creating and maintaining a growth-permissive environment for tumor cells. A growing body of work has uncovered that tumor cells recruit and educate CAFs to remodel the TME, however, the mechanisms by which this occurs remain incompletely understood. Recent studies suggest that the signal transducer and activator of transcription 3 (STAT3) is a key transcription factor that regulates the function of CAFs, and their crosstalk with tumor and immune cells within the TME. CAF-intrinsic STAT3 activity within the TME correlates with tumor progression, immune suppression and eventually the establishment of metastases. In this review, we will focus on the roles of STAT3 in regulating CAF function and their crosstalk with other cells constituting the TME and discuss the utility of targeting STAT3 within the TME for therapeutic benefit.


2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii40-iii40
Author(s):  
P Ki-Su ◽  
S Yoon ◽  
J Hwang ◽  
H Ahn

Abstract BACKGROUND The natural compound Curcumin was known to inhibit migration and invasion of glioblastoma (GBM) cells. Fascin, a kind of actin-binding proteins, is correlated with migration and invasion of GBM cells. The purpose of this study was to investigate anti-migration and anti-invasion effects of Curcumin via suppression of fascin expression in GBM cells. MATERIAL AND METHODS U87 cell line was used as an experimental model of GBM. Fascin was quantified by Western blot analysis. And, the signal transducer and activator of transcription 3 (STAT3), known to play an important role in migration and invasion of tumor cells, were analyzed by sandwich-ELISA. Migration and invasion capacities were assessed by attachment, migration and invasion assays. Cellular morphology was demonstrated by immunofluorescence. RESULTS At various concentrations of curcumin and exposure times, fascin expression decreased. After temporarily exposure to 10μM/L Curcumin during 6 hours as less invasive concentration and time, fascin expression temporarily decreased at 12 hours (18.4%, p=0.024), and since then recovered. And, the change of phosphrylated STAT3 level also reflected the temporarily decreased pattern of fascin expression at 12 hours (19.7%, p=0.010). Attachment, migration, and invasion capacities consistently decreased at 6, 12, and 24 hours. And, immunofluorescence showed the change of shape and the reduction of filopodia formation in cells. CONCLUSION Curcumin is likely to suppress the fascin expression in GBM cells, and this might be a possible mechanism for anti-migration and anti-invasion effects of Curcumin via inhibition of STAT3 phosphorylation.


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