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Oleil hydroxytyrosol (HTOL) exerts anti-myeloma activity by antagonizing key survival pathways in malignant plasma cells

ABSTRACT: Oleil hydroxytyrosol (HTOL) exerts anti-myeloma activity by antagonizing key survival pathways in malignant plasma cells

PROVIDER: PRJNA764772 | ENA |

REPOSITORIES: ENA

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Oleil hydroxytyrosol (HTOL) exerts anti-myeloma activity by antagonizing key survival pathways in malignant plasma cells

Project description:Polyphenols from olive oil are endowed with several biological activities. Chemical modifications have been recently applied to these compounds to improve their therapeutic activity in different pathological settings, including cancer. Herein, we describe the in vitro effects elicited by oleil hy-droxytyrosol (HTOL), a synthetic fatty ester of natural hydroxytyrosol with oleic acid, on multiple myeloma (MM) cells. HTOL reduced the viability of different human MM cell lines (HMCLs), triggering UPR, ER stress and apoptosis, while it was not cytotoxic against healthy peripheral blood mononuclear cells. Microarray-based whole transcriptome profiling of HTOL-treated MM cells, coupled with protein expression analyses, indicates that HTOL antagonizes molecular pathways key for malignant plasma cell survival, including the undruggable IRF4-c-MYC oncogenic axis. c-MYC gain- and loss-of-function experiments indicate that HTOL anti-tumor activity was, at least in part, due to c-MYC targeting. Taken together, these findings underscore the anti-MM activity of HTOL, providing the molecular framework for further investigation of HTOL-based treatments as novel anti-cancer agents.

2021-11-17 | GSE184489 | GEO

Oleil Hydroxytyrosol (HTOL) Exerts Anti-Myeloma Activity by Antagonizing Key Survival Pathways in Malignant Plasma Cells.

Project description:Polyphenols from olive oil are endowed with several biological activities. Chemical modifications have been recently applied to these compounds to improve their therapeutic activity in different pathological settings, including cancer. Herein, we describe the in vitro effects on multiple myeloma (MM) cells of oleil hydroxytyrosol (HTOL), a synthetic fatty ester of natural hydroxytyrosol with oleic acid. HTOL reduced the viability of various human MM cell lines (HMCLs), even when co-cultured with bone marrow stromal cells, triggering ER stress, UPR and apoptosis, while it was not cytotoxic against healthy peripheral blood mononuclear cells or B lymphocytes. Whole-transcriptome profiling of HTOL-treated MM cells, coupled with protein expression analyses, indicate that HTOL antagonizes key survival pathways for malignant plasma cells, including the undruggable IRF4-c-MYC oncogenic axis. Accordingly, c-MYC gain- and loss-of-function strategies demonstrate that HTOL anti-tumor activity was, at least in part, due to c-MYC targeting. Taken together, these findings underscore the anti-MM potential of HTOL, providing the molecular framework for further investigation of HTOL-based treatments as novel anti-cancer agents.

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CSNK1α1 mediates malignant plasma cell survival.

Project description:Here we report that targeting casein kinase 1-α1 (CSNK1α1) is a potential novel treatment strategy in multiple myeloma (MM) therapy distinct from proteasome inhibition. CSNK1α1 is expressed in all the tested MM cell lines and patient MM cells, and is not altered during bortezomib-triggered cytotoxicity. Inhibition of CSNK1α1 kinase activity in MM cells with targeted therapy D4476 or small hairpin RNAs triggers cell G0/G1-phase arrest, prolonged G2/M phase and apoptosis. D4476 also induced cytotoxicity in bortezomib-resistant MM cells and enhanced bortezomib-triggered cytotoxicity. CSNK1α1 signaling pathways include CDKN1B, P53 and FADD; gene signatures involved included interferon-α, tumor necrosis factor-α and LIN9. In addition, reduction of Csnk1α1 prevents cMYC/KRAS12V transformation of BaF3 cells independent of interleukin-3. Impartially, reducing Csnk1α1 prevented development of cMYC/KRAS12V-induced plasmacytomas in mice, suggesting that CSNK1α1 may be involved in MM initiation and progression. Our data suggest that targeting CSNK1α1, alone or combined with bortezomib, is a potential novel therapeutic strategy in MM. Moreover, inhibition of CSNK1α1 may prevent the progression of monoclonal gammopathy of undetermined significance to MM.

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