scholarly journals ARPC4 gene silencing inhibits T24 cell invasion and metastasis via a mechanism involving Arp2/3/cofilin-1 signaling pathway

2020 ◽  
Vol 19 (10) ◽  
pp. 2073-2078
Author(s):  
Shunyi Pang ◽  
Zeqin Yao ◽  
Chao Wang ◽  
Guoqiang Chen
Keyword(s):  
Cell Proliferation ◽  
Gene Silencing ◽  
Cell Invasion ◽  
Transfection Efficiency ◽  
Urinary Bladder Cancer ◽  
Short Interfering Rna ◽  
Invasion And Metastasis ◽  
T24 Cells ◽  
Protein Expressions ◽  
Interfering Rna

Purpose: To study the influence of ARPC4 gene silencing on human urinary bladder cancer (T24) cell proliferation, invasiveness and migration, and the mechanism(s) involved.Methods: Short interfering RNA (siRNA) ARPC4 silencing fragment was transfected into T24 cells. Transfection efficiency was measured with qRT-PCR. Cell proliferation, invasiveness and migratory potential were determined with CCK-8, Transwell invasion assay, and immunofluorescence assay,respectively. Protein expressions of ARPC4 and cofilin-1 were assayed using Western blotting.Results: Short interfering RNA (siRNA) silencing of ARPC4 gene led to the downregulation of mRNA and protein expressions of ARPC4 (t = 14.898, p < 0.05; t = 7.686, p < 0.05). It also significantly downregulated cofilin-1 protein, while inhibiting proliferative capacity, invasiveness and pseudopodiaformation capacity of T24 cells (t = 8.042, p < 0.05).Conclusion: The results obtained suggest that ARPC4 gene silencing inhibits T24 cell invasion and metastasis via a mechanism involving regulation of the Arp2/3/cofilin-1 signaling route. This provides new leads for gene therapy. Keywords: ARPC4, Bladder carcinoma, Gene silencing, Invasiveness, Cell proliferation

scholarly journals Effect of base modifications on structure, thermodynamic stability, and gene silencing activity of short interfering RNA

RNA ◽  
2007 ◽  
Vol 13 (8) ◽  
pp. 1301-1316 ◽  
Author(s):  
K. Sipa ◽  
E. Sochacka ◽  
J. Kazmierczak-Baranska ◽  
M. Maszewska ◽  
M. Janicka ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Thermodynamic Stability ◽  
Short Interfering Rna ◽  
Base Modifications ◽  
Interfering Rna

scholarly journals Short interfering RNA-induced gene silencing is transmitted between cells from the mammalian central nervous system

2006 ◽  
Vol 98 (5) ◽  
pp. 1541-1550 ◽  
Author(s):  
Tian-Yong Zhao ◽  
Shi-Ping Zou ◽  
Yelena V. Alimova ◽  
Guoying Wang ◽  
Kurt F. Hauser ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gene Silencing ◽  
Short Interfering Rna ◽  
Mammalian Central Nervous System ◽  
Interfering Rna

scholarly journals Suppression of short interfering RNA-mediated gene silencing by the structural proteins of hepatitis C virus

2008 ◽  
Vol 89 (11) ◽  
pp. 2761-2766 ◽  
Author(s):  
Jingmin Ji ◽  
Andrea Glaser ◽  
Marion Wernli ◽  
Jan Martin Berke ◽  
Darius Moradpour ◽  
...  
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Gene Silencing ◽  
Fluorescent Protein ◽  
Structural Proteins ◽  
Short Interfering Rna ◽  
Argonaute 2 ◽  
Co Precipitation ◽  
Green Fluorescent ◽  
Interfering Rna

Viruses have evolved strategies to overcome the antiviral effects of the host at different levels. Besides specific defence mechanisms, the host responds to viral infection via the interferon pathway and also by RNA interference (RNAi). However, several viruses have been identified that suppress RNAi. We addressed the question of whether hepatitis C virus (HCV) suppresses RNAi, using cell lines constitutively expressing green fluorescent protein (GFP) and inducibly expressing HCV proteins. It was found that short interfering RNA-mediated GFP gene silencing was inhibited when the entire HCV polyprotein was expressed. Further studies showed that HCV structural proteins, and in particular envelope protein 2 (E2), were responsible for this inhibition. Co-precipitation assays demonstrated that E2 bound to Argonaute-2 (Ago-2), a member of the RNA-induced silencing complex, RISC. Thus, HCV E2 that interacts with Ago-2 is able to suppress RNAi.

scholarly journals Gene silencing of human RAMP2 mediated by short-interfering RNA

2006 ◽  
Author(s):  
Giovanna Albertin ◽  
Maristella Ruggero ◽  
Diego Guidolin ◽  
Gastone Nussdorfer
Keyword(s):  
Gene Silencing ◽  
Short Interfering Rna ◽  
Interfering Rna

scholarly journals HIF-dependent expression of creatine kinase brain isoform (CKB) promotes breast cancer metastasis, and blocking creatine kinase activity with cyclocreatine impairs invasion and improves the efficacy of conventional chemotherapies

2021 ◽  
Author(s):  
Raisa I. Krutilina ◽  
Hilaire C. Playa ◽  
Danielle L. Brooks ◽  
Luciana P. Schwab ◽  
Deanna N. Parke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Creatine Kinase ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Kinase Activity ◽  
Creatine Kinase Activity ◽  
Breast Cancers ◽  
Invasion And Metastasis

AbstractThe oxygen-responsive Hypoxia Inducible Factor (HIF)-1 promotes several steps of the metastatic cascade. A hypoxic gene signature is enriched in triple negative breast cancers (TNBCs), which correlates with poor patient survival. Since inhibiting the HIF transcription factors with small molecules is challenging, we sought to identify genes downstream of HIF-1 that could be targeted to block invasion and metastasis. Creatine kinase brain isoform (CKB) was identified as a highly differentially expressed gene in a screen of HIF-1 wild type and knockout mammary tumor cells derived from a transgenic model of metastatic breast cancer. CKB is a cytosolic enzyme that reversibly catalyzes the phosphorylation of creatine, generating phosphocreatine (PCr) in the forward reaction, and regenerating ATP in the reverse reaction. Creatine kinase activity is inhibited by the creatine analog cyclocreatine (cCr). Loss and gain of function genetic approaches were used in combination with cCr therapy to define the contribution of CKB expression or creatine kinase activity to cell proliferation, migration, invasion, and metastasis in ER-negative breast cancers. Although tumor cell-intrinsic CKB was not essential for breast tumor cell proliferation or cell migration in vitro, CKB was necessary for cell invasion in vitro and strongly promoted tumor growth and metastasis in vivo. Similarly, cyclocreatine therapy repressed cell migration, cell invasion, formation of invadopodia, and lung metastasis. Moreover, in common TNBC cell line models, the addition of cCr to conventional agents, paclitaxel (Taxol) or doxorubicin, was either additive or synergistic to repress tumor cell growth.

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