ArticleJournal of experimental pharmacology2025
In vivo Therapeutic Inhibition of the Tp53-Induced Glycolysis and Apoptosis Regulator (TIGAR) by Intravenous Administration of an Anti-Oncological siRNA-Biopolymer, TI6752 (Tituxistatin), in a Preclinical Xenograft Model of Colorectal Cancer.
Article in Journal of experimental pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: The TP53-induced glycolysis and apoptosis regulator (TIGAR) is upregulated in many cancers and often correlates with poor clinical prognoses and serves as a key determinant of therapy-responsiveness. The TIGAR protein is structurally nearly identical to the phosphatase subunit of the bifunctional, fructose-6-phosphokinase/fructose-2,6-bisphosphatase, which has likely hindered efforts to date to develop small-molecule pharmacological inhibitors of TIGAR. Purpose: The objective of this study was to investigate the efficacy of a siRNA- Materials and Methods: The overexpression of TIGAR within K-Ras+ tumor cells and the infiltration of PECAM-1+ endothelial progenitors in primary colorectal carcinoma clinical samples were detected by immunoconfocal microscopy. Immunodeficient NIH III-nude mice were subcutaneously engrafted with HCT116 colon cancer cells and then treated with three doses of TI6752 (1 mg/kg bw) or a Vehicle control, administered intravenously at weekly intervals. The animals were humanely sacrificed and HCT116 cells within the tumor tissues were visualized using an Anti-human Ki67 primary antibody. The accumulation of biotin-labeled TI6752 within preexisting HCT116 tumor tissues, compared to other secondary organs (heart, liver, kidneys), was visualized using an AlexaFluor488-conjugated Anti-Biotin primary antibody. Results: We have shown that TIGAR is highly expressed in K-Ras+ colorectal carcinoma clinical samples and correlates with robust angiogenesis. Using a preclinical HCT116 xenograft model of colorectal carcinoma, we have demonstrated that therapeutic IV-administration of a pegylated siRNA-biopolymer, TI6752, inhibited tumor growth and reduced the infiltration of PECAM-1+ endothelial progenitors into xenograft tumor tissues without causing any adverse secondary effects. Conclusion: This study has demonstrated that IV-delivery of a pegylated siRNA-biopolymer, TI6752, targeted against
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