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Cannabichromene: Integrative modulation of apoptosis, ferroptosis, and endocannabinoid signaling in pancreatic cancer therapy

ABSTRACT: Cannabichromene: Integrative modulation of apoptosis, ferroptosis, and endocannabinoid signaling in pancreatic cancer therapy

PROVIDER: PRJNA1235622 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32681067_1.fastq.gz	Fastqsanger.gz
	SRR32681067_2.fastq.gz	Fastqsanger.gz
	SRR32681068_1.fastq.gz	Fastqsanger.gz
	SRR32681068_2.fastq.gz	Fastqsanger.gz
	SRR32681069_1.fastq.gz	Fastqsanger.gz

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Cannabichromene: Integrative modulation of apoptosis, ferroptosis, and endocannabinoid signaling in pancreatic cancer therapy

Project description:Cannabichromene (CBC: C21H3O2, M.W.: 314.46 g) is a non-psychotropic phytocannabinoid derived from Cannabis sativa (Hemp) and has been increasing attention for its potential therapeutic properties. CBC has demonstrated strong anti-inflammatory effects in animal models with edema through non-CB receptor mechanisms; however, there are still required on pharmacological studies in cancer models. In this study, we investigated the molecular mechanisms on anti-cancer activity of CBC in human pancreatic cancer cells. Through mRNA-seq analysis, we observed that many genes involved in cell death pathways were upregulated and also downregulated by CBC treatment, including ferroptosis-related genes such as HMOX1. We confirmed the functional validation of apoptosis and ferroptosis induction following CBC treatment using a variety of molecular assays. In addition, we found that CBC treatment preferentially increased the expression of TRPV1 and CB2 receptors. The cell death was reversed by inhibitor treatment on TRPV1 and CB2, suggesting that receptor expression is necessary for induction of apoptotic cell death. Finally, we confirmed the consistent regulation on apoptosis, ferroptosis, and the endocannabinoid receptors during tumor growth inhibition by CBC treatment in in-vivo xenograft models. Therefore, we propose that CBC exhibits pharmacological activity via integrative modulation for multiple cell death pathways in the pancreatic cancer therapy.

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A continuous ferroptosis-to-apoptosis landscape identifies ferroptosis biomarkers and repressors for cancer therapy

Project description:Ferroptosis, a cell death pathway driven by lipid peroxidation, is implicated in several human diseases including cancer. Although ferroptosis is entwined with apoptosis, it currently has no characteristic biomarkers or gene signature. In this project we established a continuous phenotypic gradient between ferroptosis and apoptosis and coupled it to transcriptomic and metabolomic landscapes. Omics and mechanistic studies revealed that ferroptosis was associated with enhanced MITF activity, lysosomal function, glutaminolysis, TCA cycle, and activation of ATF4, while its transition into apoptosis was attributed to enhanced ER-stress, ATF4/CHOP switch and PE/PC metabolic shift. The gradual ferroptosis-to-apoptosis transcriptomic landscape was used to generate a unique, unbiased transcriptomic predictor, the Gradient Gene Set (GGS), which classified ferroptosis and apoptosis with high accuracy. Further GGS optimization and datasets analysis of various ferroptotic and apoptotic responses revealed highly specific ferroptosis biomarkers, which were robustly validated in vitro and in vivo. A subset of the GGS was correlated with poor prognosis in breast cancer patients and in PDX models and was found to consist of different ferroptosis repressors, including PDAP1, whose knockdown suppressed breast tumor growth in a mouse model. Collectively, this study highlights molecular switches between ferroptosis and apoptosis, uncovering a highly prognostic predictive ferroptosis gene signature, pointing to a few ferroptosis repressors for targeted breast cancer therapy.

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A continuous ferroptosis-to-apoptosis landscape identifies ferroptosis biomarkers and repressors for cancer therapy

Project description:A continuous ferroptosis-to-apoptosis landscape identifies ferroptosis biomarkers and repressors for cancer therapy

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CAPG silencing promotes CRC cell apoptosis and ferroptosis via P53 pathway

Project description:Colorectal cancer (CRC) is the third most common cancer in the world and the second leading cause of cancer-related deaths. However, there are few effective therapeutic targets for colorectal cancer. Here, we report that Capping Actin Protein, Gelsolin Like (CAPG), a protein involved in actin related movement, is significantly overexpressed in human CRC tissues, and that expression levels are inversely correlated with overall survival. CAPG knockdown CRC cell lines inhibited cell proliferation, blocked cell cycle in G1 phase, increased apoptosis rate and promoted the occurrence of ferroptosis. RNA-seq data suggested that CAPG silencing promotes cell cycle arrest, apoptosis, and ferroptosis by activating the P53 pathway. Therefore, CAPG has potential to serve as a prognostic marker as well as a cancer therapy target in the future.

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2023-10-12 | PXD039297 | Pride

Silencing or amplification of endocannabinoid signaling in blastocysts via CB1 compromises trophoblast cell migration

2012-07-26 | GSE36399 | GEO

Silencing or amplification of endocannabinoid signaling in blastocysts via CB1 compromises trophoblast cell migration

Project description:Endocannabinoid signaling plays a key role in multiple events in female reproduction. In this investigation, we discovered an interesting phenomenon that mice with either elevated or silenced endocannabinoid signaling show similar defects in multiple pregnancy events, including preimplantation embryo development. To unravel the underlying mechanisms, microarray studies were was conducted using RNAs collected from WT, Cnr1-/- and Faah-/- mouse blastocysts on day 4 of pregnancy. The results show that about 100 genes showed unidirectional changes under either elevated or silenced endocannabinoid signaling. Analysis of functional grouping of these genes revealed that multiple biological functions and pathways are affected under aberrant endocannabinoid signaling, including cell migration. Several genes from the microarray data were confirmed by quantitative RT-PCR. Cell motility assays validated the predicted compromised cell migration in Cnr1-/- and Faah-/- trophoblast stem cells. This study provides molecular basis for biphasic effects of endocannabinoid signaling in female reproduction To generate Cnr1-/-, Faah-/- and WT embryos, mutant and WT females were mated with males of the same genotypes. On day 4 of pregnancy at 1500h, embryos were collected from oviducts and uteri of pregnant females, because Cnr1-/- and Faah-/- females show aberrant oviductal transport of embryos. As expected, WT embryos were mostly at the blastocyst stage and all of them were collected from uteri. However, Cnr1-/- and Faah-/- females had higher percentages of embryos at the morula stage, and some of them were still in the oviduct. Since gene expression profiles greatly vary depending on the embryonic development stage, morulae were not included in gene expression analysis; only RNAs from blastocysts were used to better understand the effects solely arising from disrupted cannabinoid signaling in blastocysts.

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CAPG silencing promotes CRC cell apoptosis and ferroptosis via P53 pathway

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