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Increasing MG1-Mediated Death in HIV-Infected Cells with SMAC Mimetics

ABSTRACT: Increasing MG1-Mediated Death in HIV-Infected Cells with SMAC Mimetics

PROVIDER: PRJNA1167326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30844040.fastq.gz	Fastqsanger.gz
	SRR30844041.fastq.gz	Fastqsanger.gz
	SRR30844042.fastq.gz	Fastqsanger.gz
	SRR30844043.fastq.gz	Fastqsanger.gz
	SRR30844044.fastq.gz	Fastqsanger.gz

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Increasing MG1-Mediated Death in HIV-Infected Cells with SMAC Mimetics

Project description:It was previously shown that interferon defects in latently HIV infected cells make them permissive to MG1 mediated killing. To increase effectiveness of MG1 therapy, we have combined MG1 with the SMAC mimetic birinapant to increase MG1 mediated killing in latently infected J1.1 cells. Increased cell death was observed compared to either treatment alone and was accompanied by increased caspase-3/7 and caspase-1 expression. However, cell death could not be blocked by the pan-caspase inhibitor ZVAD-fmk or the necroptosis inhibitor necrostatin1-s, alone or in combination, indicating that cell death does not occur via a single pathway. Furthermore, it was shown that SMAC mimetic treatment results in decreased transcription of genes that take part in the immune signalling pathway, which is likely one the ways how SMAC mimetic treament senstizes HIV infected cells to MG1 mediated death.

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SMAC mimetics induce human macrophages to phagocytose live cancer cells

Project description:Macrophages engulf apoptotic bodies and cellular debris as part of homeostasis, but they can also phagocytosis live cells such as aged red blood cells. Pharmacologic reprogramming with the SMAC mimetic LCL-161 in combination with T cell-derived cytokines can induce macrophages to phagocytosis live cancer cells in mouse models. Here we extend these findings to encompass a wide range of monovalent and bivalent SMAC mimetic compounds, demonstrating that live cell phagocytosis is a class effect of these agents. We demonstrate robust phagocytosis of live pancreatic and breast cancer cells by primary human macrophages across a range of healthy donors. Unlike mouse macrophages where combination of SMAC mimetics with lymphotoxin enhanced phagocytosis, human macrophages were more efficiently polarized to phagocytose live cells by the combination of SMAC mimetics and IFNg. We profiled phagocytic macrophages by transcriptional and proteomic methodologies, uncovering a positive feedback loop of autocrine TNFa production.

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Expression data from MDA-MB-231 parental and xenograft tumor cells treated with Smac mimetic SM-164.

Project description:Small-molecule Smac mimetics target inhibitor of apoptosis (IAP) proteins to induce TNFÎ±-dependent apoptosis in cancer cells and several Smac mimetics have been advanced into clinical development as a new class of anticancer drugs. However, preclinical studies have shown that only a small subset of cancer cell lines are sensitive to Smac mimetics used as single agents and these cell lines are at risk of developing drug resistance to Smac mimetics. Thus, it is important to understand the molecular mechanisms underlying intrinsic and acquired resistance of cancer cells to Smac mimetics in order to develop effective therapeutic strategies to overcome or prevent Smac mimetic resistance. We established Smac mimetic resistant sublines derived from MDA-MB-231 breast cancer cells, which exhibit exquisite sensitivity to the Smac mimetic SM-164, and used microarrays to detail the global programme of gene expression underlying SM-164 resistance in MDA-MB-231 cells and identified differentially expressed genes in SM-164-resistant and -sensitive MDA-MB-231 cells. SCID mice with MDA-MB-231 xenograft tumors were treated with 5 mg/kg of SM-164 intravenously for 5 days/week for 2 weeks. SM-164-regressed MDA-MB-231 tumors regrew after treatment ended. Tumor cells from these regrown MDA-MB-231 tumors were isolated and total RNAs were prepared for microarray analysis.

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Endocrine treatment potentiates antigen presentation and in combination with SMAC mimetics enhances an anti-tumor immune response in hormone receptor positive breast cancer (orig)