The cardiac glycoside deslanoside imposes an anticancer effect on prostate cancer involving multiple signaling pathways
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ABSTRACT:
PROVIDER: PRJNA764252 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15947658.fastq.gz | Fastqsanger.gz | |||
| SRR15947659.fastq.gz | Fastqsanger.gz | |||
| SRR15947660.fastq.gz | Fastqsanger.gz | |||
| SRR15947661.fastq.gz | Fastqsanger.gz | |||
| SRR15947662.fastq.gz | Fastqsanger.gz |
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Project description:Prostate cancer (PCa) is a leading cause of cancer-related deaths among men worldwide, and advanced prostate cancers are mostly incurable. It is urgently needed to find new therapeutic options. Deslanoside is a cardiac glycoside, the efficacy of which on cancers has never been reported. In this study, we investigated the effects of deslanoside on advanced PCa for the first time. RNA-sequencing results identified 141 differentially expressed mRNAs in deslanoside-treated PCa cells compared to untreated cells, which were significantly enriched in the cancer-associated pathways, including necroptosis, MAPK signaling pathway, NOD-like receptor signaling pathway, focal adhesion, small lung cancer, GnRH signaling pathway, IL-17 signaling pathway, TNF signaling pathway and apoptosis. Kaplan-Meier plotter analysis identified the effects of 11 deslanoside-influenced genes on recurrence-free survival and 4 genes on overall survival. Taken together, these results repurpose that a novel utilization of deslanoside in prostate cancer, which exerts profound inhibitory effects on advanced PCa progression.
2021-12-07 | GSE184380 | GEO
Project description:Prostate cancer (PCa) is a leading cause of cancer-related deaths among men worldwide, and novel therapies for advanced PCa are urgently needed. Cardiac glycosides represent an attractive group of candidates for anticancer repurposing, but the cardiac glycoside deslanoside has not been tested for potential anticancer activity so far. We found that deslanoside effectively inhibited colony formation in vitro and tumor growth in nude mice of PCa cell lines 22Rv1, PC-3, and DU 145. Such an anticancer activity was mediated by both the cell cycle arrest at G2/M and the induction of apoptosis, as demonstrated by different functional assays and the expression status of regulatory proteins of cell cycle and apoptosis in cultured cells. Moreover, deslanoside suppressed the invasion and migration of PCa cell lines. Genome-wide expression profiling and bioinformatic analyses revealed that 130 genes were either upregulated or downregulated by deslanoside in both 22Rv1 and PC-3 cell lines. These genes enriched multiple cellular processes, such as response to steroid hormones, regulation of lipid metabolism, epithelial cell proliferation and its regulation, and negative regulation of cell migration. They also enriched multiple signaling pathways, such as necroptosis, MAPK, NOD-like receptor, and focal adhesion. Survival analyses of the 130 genes in the TCGA PCa database revealed that 10 of the deslanoside-downregulated genes (ITG2B, CNIH2, FBF1, PABPC1L, MMP11, DUSP9, TMEM121, SOX18, CMPK2, and MAMDC4) inversely correlated, while one deslanoside-upregulated gene (RASD1) positively correlated, with disease-free survival in PCa patients. In addition, one deslanoside-downregulated gene (ENG) inversely correlated, while three upregulated genes (JUN, MXD1, and AQP3) positively correlated with overall survival in PCa patients. Some of the 15 genes have not been implicated in cancer before. These findings provide another candidate for repurposing cardiac glycosides for anticancer drugs. They also suggest that a diverse range of molecular events underlie deslanoside's anticancer activity in PCa cells.
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Project description:To find the possible signaling pathways which contribute to the anticancer effect of SW-treated HepG2 cells Global gene expression profiling is an ideal technique to obtain useful clues for exploration of the anticancer mechanism of SW. Through comparing microarray results between solvent- and SW-treated cells, differentially expressed genes were obtained (>1.5 fold). The microarray results were validated using real-time RT-PCR. We used the KEGG database, STRING database and GO database for further ananlysis, and therefore got the possible signaling pathways underlying the anticancer effect of SW. We analyzed total RNA samples of solvent- and SW-treated HepG2 cells using the Affymetrix Human Gene 1.0 ST platform. No techinical replicates were performed.
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Project description:To find the possible signaling pathways which contribute to the anticancer effect of SW-treated HepG2 cells Global gene expression profiling is an ideal technique to obtain useful clues for exploration of the anticancer mechanism of SW. Through comparing microarray results between solvent- and SW-treated cells, differentially expressed genes were obtained (>1.5 fold). The microarray results were validated using real-time RT-PCR. We used the KEGG database, STRING database and GO database for further ananlysis, and therefore got the possible signaling pathways underlying the anticancer effect of SW.
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Project description:Find the possible signaling pathways which contribute to the cell growth inhibition effect of SW-treated AGS cells Global gene expression profiling is an ideal technique to obtain useful clues for exploration of the anticancer mechanism of SW. Through comparing microarray results between solvent- and SW-treated cells, differentially expressed genes were obtained (>1.5 fold). The microarray results were validated using real-time RT-PCR. We used the KEGG database, STRING database and GO database for further ananlysis, and therefore got the possible signaling pathways underlying the anticancer effect of SW.
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Project description:Cardiac glycosides are plant-derived steroid-like compounds which have been used for the treatment of cardiovascular diseases. Ouabain, a cardiotonic steroid and specific Na+/K+-ATPase inhibitor, has been rediscovered for its potential use in the treatment of cancer. However, the cellular targets and anticancer mechanism of ouabain in various cancers remain largely unexplored. In this study, we confirmed the cytotoxic effects of ouabain on several cancer cell lines. Further examination revealed the increase of apoptosis, intracellular ROS generation and DNA double-strand breaks induced by ouabain treatment. Besides, ouabain effectively suppressed STAT3 expression as well as phosphorylation in addition to block STAT3-mediated transcription and downstream target proteins. Interestingly, these inhibitory activities seemed to be independent of the Na+/K+-ATPase. Furthermore, we found that ouabain inhibited protein synthesis through regulation of the eukaryotic initiation factor 4E (eIF4E) and eIF4E binding protein 1 (4EBP1). Taken together, our study provided a novel molecular insight of anticancer activities of ouabain in human cancer cells, which could raise the hope of using cardiac glycosides for cancer therapeutics more rational.
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Project description:This report describes our study of the efficacy and the potential mechanism underlying the anti-prion action of a new anti-prion compound having a glycoside structure in prion-infected cells. The study revealed involvements of two factors in the mechanism of the compound action: interferon and a microtubule nucleation activator, phosphodiesterase 4D interacting protein. In particular, phosphodiesterase 4D interacting protein was suggested to be important in regulating the trafficking or fusion of prion protein-containing vesicles or structures in cells. The findings of the study are expected to be useful not only for the elucidation of cellular regulatory mechanisms of prion protein, but also for the implication of new targets for therapeutic development. Prion-infected N167 cells were treated with either anti-prion glycoside compound (Gly-9) or control glycoside compound (Gly-14) at a dose of 5 M-NM-<g/mL for three days. Then, gene expression profiles were analyzed by DNA microarray analysis. Experiments were performed in quadruplicate.
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