Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The role of CDC7 in Melanoma cancer growth and progression

ABSTRACT: The role of CDC7 in Melanoma cancer growth and progression

PROVIDER: PRJNA665990 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12720780.fastq.gz	Fastqsanger.gz
	SRR12720781.fastq.gz	Fastqsanger.gz
	SRR12720782.fastq.gz	Fastqsanger.gz
	SRR12720783.fastq.gz	Fastqsanger.gz
	SRR12720784.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

The role of CDC7 in Melanoma cancer growth and progression

Project description:Disruptor of Cell Division Cycle 7 (CDC7) expression is elevated in many cancer types including melanoma. Therefore, we analyzed the role of CDC7 in melanoma. Pharmacological inhibition of CDC7 expression in Melanoma cancer cell lines resulted in decreased proliferation, and increased cell death.

2022-08-10 | GSE158621 | GEO

The role of Cdk1-cyclin B in G1/S transition revealed by chemical genetic inhibition of Cdc7

Project description:Entry of mammalian cells into DNA synthesis (S-phase) represents a key event in cell division. According to the current cell cycle models, the Cdc7 kinase represents the essential and rate-limiting trigger of DNA replication, acting together with the cyclin-dependent kinase Cdk2. Using chemical genetic systems which allow an acute shutdown of Cdc7 in in vitro cultured cells as well as in vivo in a living mouse, that Cdc7 is dispensable for cell division of many different cell types. Proteomic and phosphoproteomic analysis were performed to elucidate the compensating mechanism. We demonstrate that Cdk1-cyclin B, a kinase currently thought to act exclusively during mitosis, is also active during G1/S transition both in cycling cells and in cells exiting quiescence. We show that Cdc7 and Cdk1-cyclin B play redundant roles during G1/S transition, and at least one of these kinases is needed to allow S-phase entry. These observations revise our fundamental understanding of cell cycle progression by demonstrating that Cdk1-cyclin B physiologically regulates two distinct transitions during cell division cycle, while Cdc7 plays a redundant function in DNA replication. In TMT1, to analyze the expression of Cdc7 and its partners upon auxin-mediated induction of Cdc7 degradation, we performed a TMT analysis of ES cells treated with IAA for 24 hours. In TMT2, to analyze the phosphorylation of Cdc7 targets as a function of time upon degradation of the kinase we performed the time-resolved TMT analysis of ES cells subjected to Cdc7 degradation for three different amounts of time. In TMT3, to determine the ability of Cdk1 to phosphorylate Mcm2, we analyzed the phosphoproteome of mES cells and focused on the phosphorylation of Mcm2 upon Cdk1 inhibition.

2022-03-11 | PXD025625 | Pride

The role of UBE2T in breast cancer growth and progression

Project description:The role of UBE2T in breast cancer growth and progression

| PRJNA658487 | ENA

The role of DOT1L in ovarian cancer growth and progression

Project description:The role of DOT1L in ovarian cancer growth and progression

| PRJNA663771 | ENA

Genome-wide promoter methylation analysis associated with malignant melanoma progression

Project description:Epigenetic alterations play significant roles in the melanoma tumorigenesis and malignant progression. We profiled genome-wide promoter DNA methylation patterns of melanoma cells deribed from primary lesions of Radial Growrth phase (RGP) and Vertical Growth Phase (VGP), metastatic lesions, and primary normal melanocytes by interrogating 14,495 genes using Illumina bead chip technology. By comparative analysis of the promoter methylation profiles, we identified epigenetically silenced gene signatures that potentially associated with malignant melanoma progression. Bisulphite converted genomic DNA from a group of melanoma cells representing pathologic stages of melanoma progression (3 cell lines derived from RGP melanoma lesions, 4 cell lines derived from VGP lesions, and 3 melastatic melanomas) and normal human primary melanocytes isolated from lightly pigmented adult skin were hybridized to Illumina's Infinium HumanMethylation27 BeadChips

2013-12-20 | E-GEOD-53516 | biostudies-arrayexpress

The role of MELK in melanoma progression

Project description:Survival kinase MELK has been shown to be important for proliferation of several tumors such as brain, breast or prostate. MELK expression is elevated in cutaneous melanoma, therefore, we analyzed the role of MELK in melanoma. Inhibition of MELK in melanoma cell lines resulted in decreased proliferation, increased cell death and decreased invasion. MELK expression is regulated through MAP kinase pathway and inhibition of MAPK pathway leads to diminished MELK expression. Finally, inhibition of MELK reduces tumor size in nude mice.

2020-12-30 | GSE83907 | GEO

RNA-seq of human breast epithelial cell line MCF10A treated for 8 days with the CDC7 inhibitors XL413, TAK-931 against DMSO-treated controls

Project description:CDC7 is a serine-threonine kinase, which has an important role in the activation of replication origins in the S-phase. CDC7 is also a potential molecular target for the development of anticancer drugs. Multiple studies have shown that different cell lines have a wide range of sensitivity to CDC7 inhibition. However, how the manner in which cells respond to prolonged CDC7 inhibition has yet to be investigated. Hence, we performed an RNA-sequencing experiment to investigate variation in gene expression in cells undergoing prolonged CDC7 inhibition.

2024-05-14 | E-MTAB-13179 | biostudies-arrayexpress

Genome-wide promoter methylation analysis associated with malignant melanoma progression

2013-12-20 | GSE53516 | GEO

miR-146a Exerts Differential Effects on Melanoma Growth and Metastatization.

Project description:Malignant melanoma is the most aggressive form of skin cancer therefore it is crucial to disclose its underlying molecular mechanisms. MicroRNAs are small endogenous non-coding RNAs able to post-transcriptionally down-regulate the expression of direct target genes. Using a melanoma progression model, we identified miR-146a as a key double-acting player in melanoma malignancy. In fact, miR-146a is able to enhance tumor growth while it suppresses dissemination. We evidenced that melanoma cell growth is coordinated by its direct target lunatic fringe (LFNG) which operates on the NOTCH/PTEN/Akt pathway. Instead, metastasis formation inhibition is linked to decreased expression of ITGAV and ROCK1. Relevantly, miR-146a expression correlates with melanoma recurrence and it is enriched both in patients-derived melanoma and cutaneous metastasis samples, while its direct targets are depleted. However, miR-146a levels drop in Circulating Tumor Cells, suggesting the necessity for miR-146a expression to fluctuate during tumor progression in order to favor tumor growth and allow dissemination. This study reconciles the contradictory biological functions of miR-146a in melanoma progression and unravels distinct molecular mechanisms that need to be considered for therapeutic interventions.

2016-03-18 | GSE77090 | GEO

Transcription profiling of human melanoma progression model

Project description:Melanoma progression model

2008-06-11 | E-GEOD-1792 | biostudies-arrayexpress