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Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [seq]

ABSTRACT: The aim was to identify the effect of caspase inhibition on changes in gene expression in MCF-7 cells induced by a combination of TRAIL and LCL-161. Treated samples and control samples were collected after 24 h of treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE122979 | GEO | 2021/02/24

REPOSITORIES: GEO

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Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [array]

Project description:The aim was to identify changes in gene expression in MCF-7 cells induced by a combination of TRAIL and LCL-161. Treated samples and control samples were collected after 24 h of treatment and after 96 h of treatment followed by a three-day period in normal medium.

2022-06-30 | GSE122307 | GEO

Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161)

Project description:Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161)

| PRJNA507104 | ENA

Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [seq]

Project description:Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [seq]

| PRJNA507110 | ENA

Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [array]

Project description:Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161) [array]

| PRJNA504559 | ENA

The SMAC mimetic LCL-161 selectively targets JAK2V617F mutant cells.

Project description: Not available

| S-EPMC6941266 | biostudies-literature

Treatment of MCF-7 cells with TRAIL and Smac mimetic (LCL-161)

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-24 | GSE122980 | GEO

The SMAC mimetic LCL-161 displays antitumor activity in preclinical models of rituximab-resistant B-cell lymphoma.

Project description: Not available

| S-EPMC6290104 | biostudies-literature

The SMAC mimetic, LCL-161, reduces survival in aggressive MYC-driven lymphoma while promoting susceptibility to endotoxic shock.

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| S-EPMC4848837 | biostudies-other

Proteomic analysis of TRAIL-induced endogenous RIPK3-dependent necrosome complex

Project description:Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a well-known inducer of apoptosis via formation of the primary death-inducing signaling complex (TRAIL-DISC) at the level of membrane death receptors (DR4 and DR5) which recruit successively FADD and caspase-8. TRAIL can also induce necroptosis when caspases are inhibited. Necroptosis is a regulated cell death dependent on the formation of a cytosolic necrosome complex which includes RIPK1, RIPK3 and MLKL proteins. Elucidating the molecular mechanisms involved in TRAIL-induced necroptosis might provide new insights into the TRAIL death signaling pathway. Here, we report the analysis by mass spectrometry of endogenous RIPK3-dependent necrosome complex constituents upon necroptosis induced by TRAIL/z-VAD/Birinapant (TzB) in HT29 cells. Besides characterization of RIPK1, RIPK3, MLKL, FADD, caspase-8, we find TRIM21 as a new constituent of the necrosome complex. Moreover RIPK1, RIPK3, MLKL, P-MLKL, FADD, caspase-8 and TRIM21 are also found associated to the native TRAIL-DISC upon TzB stimulation showing initiation of the necrotic pathway at the level of TRAIL death receptors in HT29 cells. Finally, TRIM21 may positively modulate necroptosis induction by downregulating NF-kB activation.

2021-03-18 | PXD003383 | Pride

The probiotic Propionibacterium freudenreichii as a new adjuvant for TRAIL-based therapy in colorectal cancer

Project description:TRAIL (TNF-Related Apoptosis Inducing Ligand) is a well-known apoptosis inducer, which activates the extrinsic death pathway. It is pro-apoptotic on colon cancer cells, while not cytotoxic towards normal healthy cells. However, its clinical use is limited by resistance which occurs in approximately 50% of cancer cells. SCFA (Short Chain Fatty Acids) are also known to specifically induce apoptosis of cancer cells. In accordance, we have shown that food grade dairy propionibacteria induce intrinsic apoptosis of colon cancer cells, via the production and release of SCFA (propionate/acetate) acting on mitochondria. Here, we investigated possible synergistic effect between Propionibacterium freudenreichii and TRAIL. We hypothesized that acting on both extrinsic and intrinsic death pathways may exert a synergistic pro-apoptotic effect. Whole transcriptomic analysis demonstrated that propionibacterial supernatant or propionibacterial metabolites (propionate and acetate), in combination with TRAIL, boosted pro-apoptotic gene expression in HT29 human colon cancer cells. The revealed synergistic pro-apoptotic effect, depending on death receptors (TRAIL-R1/DR4, TRAIL-R2/DR5) and on caspase-8, caspase-9 and caspase-3 activation, was more lethal on cancer cells than on normal human intestinal epithelial cells (HIEC), and was inhibited by Bcl-2 expression. Finally, milk fermented only by P. freudenreichii induced apoptosis of HT29 cells and enhanced cytotoxic activity of TRAIL, as did P. freudenreichii culture supernatants or its metabolites SCFA. These results open new perspectives for the use of food grade P. freudenreichii-containing products in order to potentiate TRAIL-based cancer therapy in colorectal cancer.

2016-02-01 | GSE67033 | GEO

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