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Effect of depletion of CDK4 on gene expression of MCF-7 breast cance cells

ABSTRACT: Effect of depletion of CDK4 on gene expression of MCF-7 breast cance cells

PROVIDER: PRJNA1089108 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28372623_1.fastq.gz	Fastqsanger.gz
	SRR28372623_2.fastq.gz	Fastqsanger.gz
	SRR28372624_1.fastq.gz	Fastqsanger.gz
	SRR28372624_2.fastq.gz	Fastqsanger.gz
	SRR28372625_1.fastq.gz	Fastqsanger.gz

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Effect of depletion of CDK4 on gene expression of MCF-7 breast cance cells

Project description:CDK4/6 inhibitors act as a cytostatic by targeting CDK4/6-cyclin D, and have achieved great success in hormone receptor-positive breast cancer treatment. Beyond cell cycle signaling pathway, recent research on non-cell cycle related functions of CDK4/6 has been blooming. Insights in this field may expand the therapeutic benefits of CDK4/6 inhibitors. Here, we attempt to explore the effects of CDK4/6 inhibitors on breast cancer from the perspective of epigenetic modifications, especially histone modifications, through high-throughput proteomic and genomics approaches. We reveal that inhibition of CDK4 directly suppresses phosphorylation of p300, an acetyltransferase, stimulates its ubiquitin degradation, and down-regulates the histone H3K27ac. Then, p300-mediated transcriptionally inhibition of BRCA1 and enrichment of breast cancer stem cells (BCSC) gene signatures lead to the increase of the proportion of ALDH1+ breast CSCs in ER+ breast cancer after long treatment with CDK4/6 inhibitors in vitro and in vivo. our results reveal a novel phosphorylation substrate of CDK4/cyclin D complex, and offer an unrecognized side effect of CDK4/6 inhibitors, inducing stem cell properties in ER+ breast cancer.

2024-09-17 | GSE261797 | GEO

TRIM3 depletion in MCF-7 cells

Project description:TRIM3 depletion in MCF-7 cells

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Inhibition of GPX4 enhances CDK4/6 inhibitor activity in breast cancer.

Project description:CDK4/6 inhibition is the standard of care for estrogen receptor positive (ER+) breast cancer, although cytostasis is frequently observed, and new treatment strategies that enhance efficacy are required. We performed a genome-wide CRISPR screen to identify genetic determinants of CDK4/6 inhibitors sensitivity. Multiple genes involved in oxidative stress and ferroptosis modulated palbociclib sensitivity. Depletion or inhibition of GPX4 increased sensitivity to palbociclib in ER+ breast cancer models, and sensitised triple negative breast cancer models to palbociclib, with GPX4 null xenografts being highly sensitive to palbociclib. Palbociclib induced oxidative stress and disordered lipid metabolism with lipid peroxidation, leading to a ferroptosis-sensitive state. Lipid peroxidation relied on a peroxisome AGPAT3-dependent pathway in ER+ breast cancer models, rather than the classical ACSL4 pathway. Our data demonstrate that CDK4/6 inhibition creates vulnerability to ferroptosis that could be exploited through combination with GPX4 inhibitors, enhancing sensitivity to CDK4/6 inhibition in breast cancer.

2023-06-20 | PXD043133 | Pride

The gene expression change of RNF31 depletion in MCF-7 cells

Project description:RNF31 is atypical E3 ligase, which is highly expressed in human breast cancers. In order to understand the effect of RNF31 depletion effect in breast cancers, we knocked down the expression of RNF31 in MCF-7 cells. We aim to find the significantly changed pathways and cell biology behavior. 100uM RNF31 siRNA was applied to transfect the MCF-7 cells, while 100uM siControl was used as the control. Cells were cultured in DMEM red medium with 10% of FBS. Seventy two hours of post transfection, the total RNA was extracted to perform RNA expression analysis.

2014-02-06 | E-GEOD-46010 | biostudies-arrayexpress

Effect of JMJD2B depletion on the ER signaling pathway

Project description:JMJD2B is expressed in a high proportion of human breast tumors, and the expression levels significantly correlate with estrogen receptor (ER) positivity. To assess the effect of JMJD2B depletion on the ER signaling pathway, we performed genome-wide gene expression analysis using the Affymetrix Human Gene 1.0 ST array. RNA was extracted from steroid-depleted control MCF-7 cells (control E2(-)), control MCF-7 cells treated with E2 (control E2(+)), steroid-depleted JMJD2B-depleted MCF-7 cells (siJ2B E2(-)), and JMJD2B-depleted MCF-7 cells treated with E2 (siJ2B E2(+)).

2010-12-31 | E-GEOD-23445 | biostudies-arrayexpress

The gene expression change of RNF31 depletion in MCF-7 cells

2014-02-06 | GSE46010 | GEO

CDK4 Inactivation Hinders Cell Death and Metabolism Remodeling Mitochondria-ER contacts in Triple-Negative Breast cancer cells

Project description:The shift in the energetic demands of proliferating cells during tumorigenesis requires extensive crosstalk between the cell cycle and metabolism. Beyond their role in cell proliferation, cell cycle regulators also modulate intracellular metabolism in normal tissues. However, in the context of cancer, where CDK4 is upregulated or stabilized, the metabolic role of CDK4 is barely understood. Here, using both genetic and pharmacological approaches, we sought to determine the metabolic role of CDK4 in triple-negative breast cancer (TNBC) cells. Unexpectedly, the deletion of CDK4 only modestly reduced TNBC cell proliferation and did not hinder tumor formation in vivo. Furthermore, proapoptotic stimuli failed to induce appropriate cell death in TNBC cells upon CDK4 depletion or long-term CDK4/6 inhibitor treatment. Mechanistically, CDK4 enhances mitochondria-endoplasmic reticulum contact (MERC) formation, thereby promoting mitochondrial fission and ER-mitochondrial calcium signaling. Phosphoproteomic analysis also revealed a role for CDK4 in regulating PKA activity at MERCs to sustain ER-mitochondrial calcium signaling. Such CDK4-mediated mitochondrial calcium signaling is required for the metabolic flexibility of TNBC cells. Taken together, these results demonstrate that CDK4 inhibition leads to cell death resistance by inhibiting mitochondrial apoptosis and functions through attenuated MERCs formation and ER-mitochondrial calcium signaling in TNBC. Overall, this study provides new insights into the mechanisms of TNBC resistance to CDK4/6i therapy and paves the way to explore potential synergistic therapeutic targeting of MERCs-associated metabolic shifts.

2024-10-14 | GSE278524 | GEO

TRIM3 depletion in MCF-7 cells

Project description:We depleted TRIM3 in MCF-7 cells to check the change of the overall genomic profiling

2021-01-01 | GSE143610 | GEO

Effect of cold atmospheric plasma (CAP) on MCF-7 breast cancer cell (Illumina HumanHT-12 V4.0 beadchip)

Project description:genom-wide expression profiling of MCF-7, MCF-7 and CAP-treated MCF-7 cell. In result, cold atmospheric plasma different effect the CAP-treated MCF-7 breast cancer cell.

2019-07-26 | GSE110117 | GEO

Expression profiling of breast cancer cell lines MCF-7 and MCF-7R4

Project description:Human breast cancer cell line MCF-7 is usually sensitive to chemotherapy drug BMS-554417, an insulin receptor (IR) and insulin-like growth factor receptor (IGFR) inhibitor. However, through step-wise increase in BMS-554417 doses in culture media, we were able able to screen and select a single MCF-7 clone that is BMS-554417 resistant. It is cross resistant to BMS-536924. This new line of MCF-7 cells was named as MCF-7R4. The transcriptome profiling of both MCF-7 and MCF-7R4 was performed using Affymetrix HG-U133 plus2.0 GeneChip arrays.

2009-11-06 | GSE18912 | GEO

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