scholarly journals Piwil2 Suppresses P53 by Inducing Phosphorylation of Signal Transducer and Activator of Transcription 3 in Tumor Cells

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30999 ◽  
Author(s):  
Yilu Lu ◽  
Kun Zhang ◽  
Chao Li ◽  
Youlin Yao ◽  
Dachang Tao ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Signal Transducer ◽  
Transcription 3

scholarly journals Exploiting the STAT3 Nexus in Cancer-Associated Fibroblasts to Improve Cancer Therapy

2021 ◽  
Vol 12 ◽  
Author(s):  
Amr Allam ◽  
Marina Yakou ◽  
Lokman Pang ◽  
Matthias Ernst ◽  
Jennifer Huynh
Keyword(s):  
Tumor Cells ◽  
Immune Suppression ◽  
Immune Cells ◽  
Therapeutic Benefit ◽  
Cancer Associated Fibroblasts ◽  
Signal Transducer ◽  
Growing Body ◽  
Heterogenous Population ◽  
Transcription 3 ◽  
Soluble Components

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.

scholarly journals P10.01 Anti-migration and anti-invasion effects of curcumin via suppression of fascin expression in glioblastoma cells

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii40-iii40
Author(s):  
P Ki-Su ◽  
S Yoon ◽  
J Hwang ◽  
H Ahn
Keyword(s):  
Western Blot ◽  
Tumor Cells ◽  
Natural Compound ◽  
Sandwich Elisa ◽  
Actin Binding ◽  
Migration And Invasion ◽  
Signal Transducer ◽  
Stat3 Phosphorylation ◽  
Transcription 3 ◽  
Invasion Assays

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.

scholarly journals Targeting STAT3 in Cancer with Nucleotide Therapeutics

Cancers ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 1681 ◽  
Author(s):  
Yue-Ting K. Lau ◽  
Malini Ramaiyer ◽  
Daniel E. Johnson ◽  
Jennifer R. Grandis
Keyword(s):  
Nucleic Acid ◽  
Tumor Cells ◽  
Target Genes ◽  
Critical Role ◽  
Signal Transducer ◽  
Clinical Testing ◽  
Antisense Molecule ◽  
Novel Approaches ◽  
Transcription 3 ◽  
Stat3 Decoy

Signal transducer and activator of transcription 3 (STAT3) plays a critical role in promoting the proliferation and survival of tumor cells. As a ubiquitously-expressed transcription factor, STAT3 has commonly been considered an “undruggable” target for therapy; thus, much research has focused on targeting upstream pathways to reduce the expression or phosphorylation/activation of STAT3 in tumor cells. Recently, however, novel approaches have been developed to directly inhibit STAT3 in human cancers, in the hope of reducing the survival and proliferation of tumor cells. Several of these agents are nucleic acid-based, including the antisense molecule AZD9150, CpG-coupled STAT3 siRNA, G-quartet oligodeoxynucleotides (GQ-ODNs), and STAT3 decoys. While the AZD9150 and CpG-STAT3 siRNA interfere with STAT3 expression, STAT3 decoys and GQ-ODNs target constitutively activated STAT3 and modulate its ability to bind to target genes. Both STAT3 decoy and AZD9150 have advanced to clinical testing in humans. Here we will review the current understanding of the structures, mechanisms, and potential clinical utilities of the nucleic acid-based STAT3 inhibitors.

Hypoxia is a potent inducer of the iron masterswitch hepcidin via Signal Transducer and Activator of Transcription 3 (STAT3)

2017 ◽  
Author(s):  
I Silva ◽  
V Rausch ◽  
T Peccerella ◽  
G Millonig ◽  
HK Seitz ◽  
...  
Keyword(s):  
Signal Transducer ◽  
Potent Inducer ◽  
Transcription 3

Magnesium-dependent Phosphatase (MDP) 1 is a Potential Suppressor of Gastric Cancer

2019 ◽  
Vol 19 (10) ◽  
pp. 817-827
Author(s):  
Jianbo Zhu ◽  
Lijuan Deng ◽  
Baozhen Chen ◽  
Wenqing Huang ◽  
Xiandong Lin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Dna Methylation ◽  
Cell Proliferation ◽  
Protein C ◽  
Biological Function ◽  
Prognostic Markers ◽  
Biological Effects ◽  
Signal Transducer ◽  
Gastric Cancer Cells ◽  
Transcription 3

Background:Recurrence is the leading cause of treatment failure and death in patients with gastric cancer (GC). However, the mechanism underlying GC recurrence remains unclear, and prognostic markers are still lacking.Methods:We analyzed DNA methylation profiles in gastric cancer cases with shorter survival (<1 year) or longer survival (> 3 years), and identified candidate genes associated with GC recurrence. Then, the biological effects of these genes on gastric cancer were studied.Results:A novel gene, magnesium-dependent phosphatase 1 (mdp1), was identified as a candidate gene whose DNA methylation was higher in GC samples from patients with shorter survival and lower in patients with longer survival. MDP1 protein was highly expressed in GC tissues with longer survival time, and also had a tendency to be expressed in highly differentiated GC samples. Forced expression of MDP1 in GC cell line BGC-823 inhibited cell proliferation, whereas the knockdown of MDP1 protein promoted cell growth. Overexpression of MDP1 in BGC-823 cells also enhanced cell senescence and apoptosis. Cytoplasmic kinase protein c-Jun N-terminal kinase (JNK) and signal transducer and activator of transcription 3 (Stat3) were found to mediate the biological function of MDP1.Conclusion:These results suggest that MDP1 protein suppresses the survival of gastric cancer cells and loss of MDP expression may benefit the recurrence of gastric cancer.

Sign in / Sign up

Export Citation Format

Share Document