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Effects of AKT/WEE1 inhibitors or ALDH inhibitor combined with PD-1 antibody on melanoma

ABSTRACT: Effects of AKT/WEE1 inhibitors or ALDH inhibitor combined with PD-1 antibody on melanoma

PROVIDER: PRJNA818337 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18402583.fastq.gz	Fastqsanger.gz
	SRR18402584.fastq.gz	Fastqsanger.gz
	SRR18402585.fastq.gz	Fastqsanger.gz
	SRR18402586.fastq.gz	Fastqsanger.gz
	SRR18402587.fastq.gz	Fastqsanger.gz

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Effects of AKT/WEE1 inhibitors or ALDH inhibitor combined with PD-1 antibody on melanoma

Project description:The effects of AKT/WEE1 inhibitors or ALDH inhibitor combined with PD-1 antibody on melanoma were examined. Mouse B16F10 melanoma cells were subcutaneously injected into C57/B6 mice. When tumors were well-vascularized, mice were treated with anti-PD-1, AKT I (AZD5363)+WEE1 I (MK1775), AZD5363+MK1775+anti-PD-1, ALDH I (KS100), KS100+ anti-PD-1 daily. Mice were sacrificed when tumors in the control group (DMSO treated) reached 2000 mm3 and tumors were removed. RNA was extracted from tumor samples and gene expression was analized using RNAseq analysis.

2023-12-31 | GSE199096 | GEO

ALDH RNA seq

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Expression data from ALDH− and ALDH+ shXIst0SUM159 cells treated with or without DOX

Project description:We used microarrays to identify differentially expressed miRNAs in ALDH− and ALDH+ cells treated with or without DOX

2023-08-02 | GSE222742 | GEO

Wee1 Inhibition sensitizes prostate cancer cells to Hsp90 inhibitor to activate the intrinsic apoptotic pathway

Project description:Heat shock protein 90 (Hsp90) is an essential evolutionarily conserved molecular chaperone in eukaryotes. Cancer cells rely on Hsp90 to chaperone activated oncoproteins, and its involvement in numerous signaling pathways makes it an attractive target for drug development. Surprisingly, however, the impact of Hsp90 inhibitors on cancer cells is most commonly cytostatic, and efforts to enhance the anti-tumor activity of Hsp90 inhibitors in the clinic remain a significant challenge. In this study, we show that dual inhibition of Wee1 tyrosine kinase and Hsp90 causes prostate cancer cells to undergo apoptosis. Gene-expression profiling revealed that induction of the intrinsic apoptotic pathway by this drug combination coincided with transcriptional down-regulation of Survivin and Wee1, an outcome not seen in cells treated separately with either agent. At the translational level, expression of these two proteins as well as activated Akt was completely abrogated. Similar results were obtained in prostate cancer xenografts. These data establish a novel therapeutic strategy to enhance the efficacy of Hsp90 inhibitors in prostate cancer, and they provide a mechanistic rationale for stimulating the pro-apoptotic activity of Hsp90 inhibitors. In order to explore the mechanism underlying the enhanced cell death caused by Wee1 inhibitorII and 17-AAG combination, we performed microarray analysis using PC3 cells treated with Wee1 inhibitorII alone, 17-AAG alone, or the two drugs in combination. There are 12 samples in total. There are three experimental replicate. Samples 1, 5 and 9 are control (C) (untreated PC3- prostate cancer cells). Samples 2, 6, and 10 are cells treated with Wee1 inhibitor II (W). Samples 3, 7, and 11 are treated with 17-AAG (A), (an Hsp90 inhibitor). Samples 4, 8, and 12 are treated with both Wee1 inhibitorII and 17-AAG (WA). Samples 5 was removed from our analysis due to weak signal.

2013-01-10 | E-GEOD-38972 | biostudies-arrayexpress

Human colorectal cancer cell line CRC#21: ALDH-high cells vs. ALDH-low cells

Project description:Transcriptional profiling of cancer stem cells (ALDH-high cells) comparing non-cancer stem cells (ALDH-low cells), sorted out using ALDEFLUOR assay. Goal was to identity cancer stem cell-specific genes. Two-condition experiment, sphere-cultured cells vs. adherent-cultured cells: 1 ALDH-high replicate and 1 ALDH-low replicate.

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ALDH-positive MCF-7 cells

Project description:We used an Aldefluor assay system to study the signaling pathways that regulate the frequency and maintenance of ALDH-positive cell population in MCF-7 cells as a CSC model. Through microarray analysis, we investigated a possible receptor that increases the proportion of the ALDH-positive cell population in MCF-7 cells. MCF-7 were stained with Aldefluor and ALDH-positive cells were sorted using flow cytometry. Gene expression profiles of ALDH+ cells were compared with ALDH- cells.

2014-09-23 | E-GEOD-59653 | biostudies-arrayexpress

RNASeq analysis of human ALDH- and ALDH+ DU145 xenografts in nu/nu mice upon radiotherapy treatment

Project description:Purpose: we aimed at identify and compare the transcriptional changes of ALDH- and ALDH+ DU145 xenografts upon radiotherapy treatment. Method: Xenografts were generated by injection of ALDH- and ALDH+ DU145 cells in male NMRI-Foxn1 nu/nu immune-deficient mice and subjected to fractionated irradiation to a final dose of 50 Gy. Tumors were excised and processed for total RNA extraction and RNAseq analysis.

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Evaluation of gene expression between ALDH-high and ALDH-low cells in endometrial cancer-derived spheroids

Project description:To identify genes that are differentially expressed between ALDH-high and ALDH-low cells in endometrial cancer-derived spheroids, we performed whole genome microarray expression profiling as a discovery platform. Human endometrial cancer stem spheroid cells from three patients were sorted into ALDH-high and ALDH-low cells using the FACS Aria II Cell Sorter. Total RNA extracted from the cells were labeled with Cy3 and used for microarray analyses with Agilent Whole Human Genome Oligo Microarrays.

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Human colorectal cancer cell line CRC#21: ALDH-high cells vs. ALDH-low cells

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TRRAP-mediated regulation of Wee1

Project description:The G2 DNA damage checkpoint inhibits Cdc2 and mitotic entry through the dual regulation of Wee1 and Cdc25 by the Chk1 effector kinase. Up-regulation of Chk1 by mutation or overexpression bypasses the requirement for up-stream regulators or DNA damage to promote a G2 cell cycle arrest. We screened in fission yeast for mutations that rendered cells resistant to overexpressed Chk1. We identified a mutation in tra1, which encodes one of two homologs of TRRAP, an ATM/R-related pseudokinase that scaffolds several histone acetyltransferase (HAT) complexes. Inhibition of histone deacetylases reverts the resistance to overexpressed Chk1, suggesting this phenotype is due to a HAT activity, though expression of checkpoint and cell cycle genes is not greatly affected. Cells with mutant or deleted tra1 activate Chk1 normally and are checkpoint proficient. However, these cells are semi-wee even when overexpressing Chk1, and accumulate inactive Wee1 protein. The Cdr (changed division response) kinases Cdr1 and Cdr2 are negative regulators of Wee1, and while best characterized in the cellular response to limited nutrition, we show that they are required for the Tra1-dependent alterations to Wee1 function. This identifies Tra1 as another component controlling the timing of entry into mitosis via Cdc2 activation. Two and three independent microaaray experiments were done for wild type and the mutant (tra1-1) respectively.

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