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Impact of Palbociclib (PD-0332991 CDK4/6 inhibitor) on gene expression of MCF7 cells

ABSTRACT: Impact of Palbociclib (PD-0332991 CDK4/6 inhibitor) on gene expression of MCF7 cells

PROVIDER: PRJNA985731 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24978566.fastq.gz	Fastqsanger.gz
	SRR24978567.fastq.gz	Fastqsanger.gz
	SRR24978568.fastq.gz	Fastqsanger.gz
	SRR24978569.fastq.gz	Fastqsanger.gz
	SRR24978570.fastq.gz	Fastqsanger.gz

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Impact of Palbociclib (PD-0332991; CDK4/6 inhibitor) on gene expression of MCF7 cells

Project description:Studying DNA damage-induced senescence, we observed a similar phenotype upon CDK4/6 inhibition in breast cancer cells. We used RNA sequencing to investigate the gene expression profile of MCF7 cells upon CDK4/6 inhibition five days after exposure.

2024-07-17 | GSE235350 | GEO

Gene expression profiling of HepG2 cells after treatment of PD-0332991 and CDK4-6 Knockdown

Project description:The aim of this study is to estimate gene expression variations involved in glucose meatbolism in HepG2 cell line after cell cycle(G1 to S phase) inhibition by using drug(PD-0332991) or CDK4-6-knock down. We hypothesized that transition of glycolytic gene expression might indicates the effect of PD-0332991 drug treatment in Hepatocellular carcinoma cells.

2020-02-18 | GSE145389 | GEO

CDK4/6 inhibitors in ER positive breast cancers

Project description:Gene expression levels were determined with control or PD-0332991 treatment MCF7, T47D cells were subject to DMSO/ PD-0332991 treatment . RNA was harvested at 120 hours post treatment and analyzed on Illumina microarrays

2016-08-01 | E-GEOD-80987 | biostudies-arrayexpress

Gene expression alterations associated with acquired-resistance to the CDK4/6 inhibitor palbociclib [Palbociclib resistance_RNASeq]

Project description:RNA-seq was performed to compare the transcriptional programmes of palbociclib-resistant A375 and CHL1 cells compared to their parental counterparts Cyclin dependent kinase 4/6 (CDK4/6) inhibitors are an established treatment in estrogen receptor positive breast cancer and are currently in clinical development in melanoma; a tumour that exhibits high rates of CDK4 activation. We analyzed melanoma cells with acquired resistance to the CDK4/6 inhibitor palbociclib, and demonstrated that palbociclib-mediated inhibition of PRMT5 is essential for sensitivity to CDK4/6 inhibitors. Mechanistically, by inhibiting PRMT5 activity, palbociclib alters MDM4 pre-mRNA splicing leading to decreased MDM4 protein expression and subsequent p53 activation. In turn, p53 increases p21 leading to inhibition of CDK2, the main kinase substituting for CDK4/6 and a key driver of resistance to palbociclib. Loss of the ability of palbociclib to regulate the PRMT5-MDM4 axis leads to resistance. Importantly, combining palbociclib with the PRMT5 inhibitor GSK3326595 enhances the efficacy of palbociclib in treatment naïve and resistant models and also delays the emergence of resistance. Our studies have uncovered a novel mechanism of action of CDK4/6 inhibitors in regulating the MDM4 oncogene and the tumor suppressor, p53. Furthermore, we have established that palbociclib inhibition of the PRMT5-MDM4 axis is essential for robust melanoma cell sensitivity and provide pre-clinical evidence that co-inhibition of CDK4/6 and PRMT5 is an effective and well tolerated therapeutic strategy. Overall our data provides a strong rationale for further investigation of novel combinations of CDK4/6 and PRMT5 inhibitors in not only melanoma but other tumour types including breast, pancreatic and esophageal carcinoma.

2019-08-23 | GSE133567 | GEO

Effects of PD-0332991 on gene expression of human pancreatic ductal adenocarcinoma (PDAC) cell lines

Project description:PD-0332991 is a small molecule inhibitor for Cdk4 and Cdk6. It exerted growth inhibitory effects on PDAC cell lines (AsPC-1 and COLO-357). Microarray analysis was used to characterize the changes in gene expression profiles of AsPC-1 and COLO-357 upon PD-0332991 incubation AsPC-1 and COLO-357 cells were treated in the absence or presence of 5 ÂµM PD-0332991 for 24 h and 72 h. Each expreimental condition had biological triplicates. Twenty-four samples were analyzed in total.

2012-10-10 | E-GEOD-39646 | biostudies-arrayexpress

Effects of PD-0332991 on gene expression of human pancreatic ductal adenocarcinoma (PDAC) cell lines

2012-10-10 | GSE39646 | GEO

Expression data from vehicle or PD-0332991 treated human T-ALL lines

Project description:Cyclin D3 is critical hematopoiesis and loss of cyclin D3 leads to resistance to transformation of bone marrow progenitors by Notch1-IC. We used a small molecule targeting cyclin D3:CDK4/6 activity to study whether its inhibition is an effective therapeutic strategy. We analyzed T-ALL lines in vitro with PD-0332991 or vehicle control to determine genes affected by the drug. CEM, Jurkat, DND41, and CUTL-1 cell lines were treated with 1 uM PD-0332991 or DMSO for 15 hours prior to RNA extraction and hybridization to Human Genome U133 Plus 2.0 Affymetrix arrays.

2012-12-13 | E-GEOD-40635 | biostudies-arrayexpress

Prolonged halting of gene expression in early G1 arrest by inhibition of CDK4/CDK6 reprograms myeloma cells for cytotoxic killing

Project description:By selective and reversible inhibition of CDK4/CDK6, we have developed a strategy to both inhibit proliferation and enhance cytotoxic killing of cancer cells. Induction of prolonged early-G1 arrest (pG1) by CDK4/CDK6 inhibition halts gene expression in early-G1 and prevents expression of genes programmed for other cell cycle phases. S-phase synchronization upon removal of the early-G1 block (pG1-S) fails to completely restore scheduled gene expression. Consequently, coordinate loss of IRF4 and gain of Bim and Noxa expression sensitize myeloma tumor cells to bortezomib-induced apoptosis in pG1 and more profoundly in pG1-S in vitro. Induction of pG1 and pG1-S by CDK4/CDK6 inhibition augments tumor-specific bortezomib killing in myeloma xenografts. Inhibition of CDK4/CDK6 in combination therapy thus represents a novel mechanism-based cancer therapy. PD 0332991 (PD) is the only known specific and reversible CDK4/CDK6 inhibitor. Gene expression was measured in myeloma MM1.S cells treated with PD (0.25 uM) in triplicate for 12, 24 or 36 h, or in cells released from G1, induced by 24hPD, for 4 or 18 h.

2012-04-06 | E-GEOD-35728 | biostudies-arrayexpress

Stromal senescence following treatment with the CDK4/6 inhibitor palbociclib increases mammary cancer metastasis

Project description:One potential resistance mechanism to CDK4/6 inhibitors in breast cancer could be induction of cellular senescence in normal host tissues. The aim of our study was to identify CDK4/6 inhibition-induced changes to host tissues that impact metastasis. Using mouse models, we found that pre-treatment with palbociclib can increase metastatic seeding of mouse mammary cancer cells in the lungs and that this can be mitigated by eliminating senescent host cells. We describe palbociclib-induced gene expression changes in lungs that correlate with this effect and reveal altered intra-lung immune populations. Senescent endothelial cells are identifiable within lung metastases of mice pre-treated with palbociclib. Using in vitro models, we show that palbociclib treatment increases endothelial cell senescence and affects macrophage invasion and migration. These studies describe how CDK4/6 inhibition-induced cellular senescence in host tissues affects metastasis and disease progression in breast cancer, which remain key obstacles to achieving long-term survival.

2023-04-04 | GSE223759 | GEO

RNA-seq of human breast cancer cell lines MCF7 and T74D naive and resistant to palbociclib treated with capivasertib, fulvestrant and combination

Project description:T47D and MCF7 cell lines were treated with long-term (continuous) palbociclib to induce 4 resistant cell-lines (T47D RB-, T47D CDK6H, MCF7 RB- and MCF7 PacqR). Each cell line (both parental and resistant) were then treated with DMSO (control), capivasertib monotherapy, fulvestrant monotherapy and capivasertib/fulvestrant combination. RNA data is available after each treatment and resistant cell lines additionally have RNA data available after continuous palbociclib treatment.

2023-08-14 | E-MTAB-13262 | biostudies-arrayexpress

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