Melanoma tumor growth and progression are highly dependent on adequate blood supply through angiogenesis. Since several genes involved in angiogenesis revealed potential binding sites for the transcription factor Sp1, we have examined the effects of local inoculation of Sp1 decoy oligodeoxynucleotides (ODNs) on the growth of transplanted murine melanoma tumors and the expression of VEGF and TNF-alpha within these tumors. Treatment with Sp1 decoy ODNs, but not their mutated form, led to a significant increase (P=0.041) of the tumor necrotic area, as evaluated morphometrically. Tumor necrosis was associated with a significant decrease of microvascular density (P=0.012) and relative vascular area (P=0.026), as determined by counting CD34-positive vascular structures within the tumor microenvironment of Sp1 decoy ODNs and control ODN-treated tumors. RT-PCR experiments showed a strong decrease in the levels of VEGF188 and VEGF164 isoforms and a moderate decrease of TNF-alpha in Sp1 decoy-treated tumors. Taken together, our results indicate that Sp1 decoy ODNs may inhibit angiogenesis by affecting the gene expression of key players in angiogenesis such as TNF-alpha and VEGF. These findings indicate that Sp1 decoy ODNs may be a potential new therapeutic tool in antiangiogenic therapy.
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http://dx.doi.org/10.1038/sj.gt.3302111 | DOI Listing |
Int Immunopharmacol
July 2024
Laboratory of Risks Related to Environmental Stresses: Fight and Prevention, Unit UR03ES06, Faculty of Sciences of Bizerte, University of Carthage, Tunisia.
This report drives insights for the investigation of the underlying mechanisms of antitumor effects of Teucrium ramosissimum (TrS) essential oil (EO) that elicits colon tumor protection via activation of cell death machinery. A study of the aerial part phytocomplex was performed by FTIR spectra and GC/MS. In vivo colon carcinogenesis induced by LPS was carried out using mouse model.
View Article and Find Full Text PDFSci China Life Sci
July 2024
State Key Laboratory of Agricultural Microbiology, Hubei Hongshan Laboratory, Frontiers Science Center for Animal Breeding and Sustainable Production, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan, 430070, China.
Dietary exposure to aflatoxin B (AFB) is harmful to the health and performance of domestic animals. The hepatic cytochrome P450s (CYPs), CYP1A1 and CYP2A6, are the primary enzymes responsible for the bioactivation of AFB to the highly toxic exo-AFB-8,9-epoxide (AFBO) in chicks. However, the transcriptional regulation mechanism of these CYP genes in the liver of chicks in AFB metabolism remains unknown.
View Article and Find Full Text PDFAging (Albany NY)
September 2021
Laboratory of Biochemistry and Molecular Biology, University of Carthage, Faculty of Sciences of Bizerte, Zarzouna, Bizerte 7021, Tunisia.
Background: The aim of the study is to determine the anticancer activity of (TS) and its underlying mechanisms using and in animal models.
Methods: HCT116 cells were treated with TS essential oil alone or with TRAIL, and then its anticancer effect was determined by using MTT assay, live dead assay, caspase activation and PARP cleavage. Further mechanisms of its anticancer effects was determined by analyzing expression of death receptor signaling pathway using Western blotting.
Front Biosci (Schol Ed)
June 2021
Laboratory of Biochemistry and Molecular Biology, Faculty of Sciences of Bizerte, University of Carthage, Tunisia.
TNF-related apoptosis-inducing ligand (TRAIL/Apo2L), a member of cytokine family, is known to selectively induce apoptosis in cancer cells. However, developing resistance to TRAIL is a major obstacle in cancer therapy. In this study, the effect of (TA) essential oil on inhibition of cancer cell growth and enhancing TRAIL-induced apoptosis were investigated in colon cancer cells.
View Article and Find Full Text PDFBiochim Biophys Acta Gen Subj
September 2020
Department of Biophysics, Bose Institute, Centenary Campus, P-1/12, C.I.T. Scheme VIIM, Kankurgachi, Kolkata 700054, India. Electronic address:
Background: The transcription-inhibitory G-Quadruplex(Pu27-GQ) at c-MYC promoter is challenging to target due to structural heterogeneity. Nucleoside diphosphate kinase (NM23-H2) specifically binds and unfolds Pu27-GQ to increase c-MYC transcription. Here, we used Inosine 5'-diphosphate (IDP) to disrupt NM23-H2-Pu27-GQ interactions and arrest c-MYC transcription without compromising NM23-H2-mediated kinase properties.
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