Presenting Author

Mohammed Sikander

Presentation Type

Oral Presentation

Discipline Track

Biomedical Science

Abstract Type

Research/Clinical

Abstract

Aberrant activation of β-catenin signaling is strongly associated with cancer proliferation, invasion, migration, and metastasis, thus small molecules that can inhibit this pathway might have great clinical significance. Our molecular modeling studies suggest that Ormeloxifene (ORM), a triphenylethylene molecule docks with β-catenin, and its brominated analogue (Br-ORM) bind more effectively with relatively less energy (-7.6 kcal/mol) to the active site of β-catenin as compared to parent ORM. Herein, we report the synthesis and characterization of a Br-ORM by NMR and FTIR, as well as its anti-cancer potential in cervical cancer models in vitro and in vivo. Br-ORM treatment effectively inhibited tumorigenic features (cell proliferation and colony forming ability, etc.) and induced apoptotic death as evident by pronounced PARP-cleavage and arrest of cells in G1-S phase of cell cycle. Further, mechanistic investigations revealed that Br-ORM targets the key proteins involved in promoting epithelial mesenchymal transition (EMT) as demonstrated by upregulation of E-cadherin expression and repression of N-cadherin, Vimentin, Snail, MMP-2, -9 expression. Br-ORM also represses the expression and nuclear subcellular localization of β-catenin. Consequently, Br-ORM treatment effectively inhibited tumor growth in orthotopic cervical cancer xenograft mouse model along with EMT associated changes as compared to vehicle control treated mice. Altogether, our in vitro and pre-clinical in vivo findings suggest that Br-ORM is a novel, promising β-catenin inhibitor, therefore can be harnessed as a potent anti-cancer small molecule for the treatment of aberrant wnt/β-catenin signaling induced cancers, including cervical cancer.

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Novel therapeutic strategy for cervical cancer treatment

Aberrant activation of β-catenin signaling is strongly associated with cancer proliferation, invasion, migration, and metastasis, thus small molecules that can inhibit this pathway might have great clinical significance. Our molecular modeling studies suggest that Ormeloxifene (ORM), a triphenylethylene molecule docks with β-catenin, and its brominated analogue (Br-ORM) bind more effectively with relatively less energy (-7.6 kcal/mol) to the active site of β-catenin as compared to parent ORM. Herein, we report the synthesis and characterization of a Br-ORM by NMR and FTIR, as well as its anti-cancer potential in cervical cancer models in vitro and in vivo. Br-ORM treatment effectively inhibited tumorigenic features (cell proliferation and colony forming ability, etc.) and induced apoptotic death as evident by pronounced PARP-cleavage and arrest of cells in G1-S phase of cell cycle. Further, mechanistic investigations revealed that Br-ORM targets the key proteins involved in promoting epithelial mesenchymal transition (EMT) as demonstrated by upregulation of E-cadherin expression and repression of N-cadherin, Vimentin, Snail, MMP-2, -9 expression. Br-ORM also represses the expression and nuclear subcellular localization of β-catenin. Consequently, Br-ORM treatment effectively inhibited tumor growth in orthotopic cervical cancer xenograft mouse model along with EMT associated changes as compared to vehicle control treated mice. Altogether, our in vitro and pre-clinical in vivo findings suggest that Br-ORM is a novel, promising β-catenin inhibitor, therefore can be harnessed as a potent anti-cancer small molecule for the treatment of aberrant wnt/β-catenin signaling induced cancers, including cervical cancer.

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