Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Ribociclib derivative Rib-CA suppresses breast cancer progression by inducing p53-dependent apoptosis

ABSTRACT: Ribociclib derivative Rib-CA suppresses breast cancer progression by inducing p53-dependent apoptosis

PROVIDER: PRJNA1248440 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR33045942_1.fastq.gz	Fastqsanger.gz
	SRR33045942_2.fastq.gz	Fastqsanger.gz
	SRR33045943_1.fastq.gz	Fastqsanger.gz
	SRR33045943_2.fastq.gz	Fastqsanger.gz
	SRR33045944_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Ribociclib derivative Rib-CA suppresses breast cancer progression by inducing p53-dependent apoptosis

Project description:RNA sequencing and bioinformatics analysis revealed 2628 differentially expressed genes, with functional enrichment indicating strong associations with the p53 pathway, apoptosis, and G2/M checkpoint regulation

2025-04-09 | GSE294138 | GEO

Ribociclib Derivative RB-BC Induces Apoptosis in Breast Cancer through p53 Pathway Activation

Project description:Breast cancer persists as the most prevalent malignancy and principal contributor to cancer-associated mortality among women worldwide, exhibiting marked disease heterogeneity and therapeutic resistance. Consequently, the development of novel therapeutic agents remains imperative. Ribociclib, a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor, has emerged as a focus in adjuvant breast cancer research due to its mechanism of cell cycle arrest induction.Building upon this rationale, we designed and synthesized a novel ribociclib derivative RB-BC, systematically investigating its anti-neoplastic efficacy and molecular mechanisms in breast cancer through integrated in vitro and in vivo experimental systems. The compound's anti-proliferative effects were quantitatively assessed via MTT assays , EdU incorporation assays , and colony formation assays .Functional characterization through cell adhesion assays, scratch wound healing assays, and Transwell invasion assays demonstrated RB-BC’s dose-dependent suppression of tumor migration and invasion. Mechanistic analyses via RNA sequencing and Western blotting revealed that its anti-tumor activity primarily stems from p53 pathway activation, inducing caspase-3-mediated apoptosis in breast cancer cells. Machine learning algorithms identified p53-associated genetic signatures, and subsequent bioinformatics analyses elucidated their significant correlation with immune cell infiltration dynamics in the tumor microenvironment (TME).Moreover, RB-BC effectively suppressed tumor growth in vivo and significantly disrupted angiogenesis in the chick chorioallantoic membrane (CAM) assay. In summary, the ribociclib-derived compound RB-BC demonstrates compelling potential as a candidate therapeutic agent for breast cancer.

2025-04-15 | GSE294486 | GEO

A novel Ribociclib derivative, YW-LF, exerts anti-breast cancer effects by activating the p53 pathway.

Project description:Breast cancer remains the most prevalent malignancy among women worldwide. Although ribociclib, a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor, has demonstrated significant antitumor activity in breast cancer therapy, its clinical application is limited by hematological toxicity, cardiotoxicity, and patient tolerance. In this study, we synthesized a novel ribociclib derivative, YW-LF, and systematically evaluated its antitumor activity and underlying mechanisms. Through a series of in vitro assays—including MTT, colony formation, EdU incorporation, transwell migration, and invasion experiments—as well as in vivo evaluation using a chick chorioallantoic membrane (CAM) model, we demonstrated that YW-LF significantly inhibited breast cancer cell proliferation, migration, and invasion, while effectively suppressing tumor growth and angiogenesis. Compared to the positive control ribociclib, YW-LF exhibited superior antitumor efficacy. Transcriptomic profiling revealed that YW-LF suppressed tumor progression by activating the p53 signaling pathway and apoptosis-related pathways. Western blot analysis further validated the dysregulation of key proteins, providing protein-level evidence for its mechanism of action. Additionally, machine learning-based bioinformatics analysis identified three core genes (ADRB1, ATOH8, and CCNE2) with potential clinical significance in breast cancer diagnosis and treatment. Immune infiltration analysis highlighted the strong correlation of these genes with specific immune cell subsets within the tumor microenvironment, underscoring their critical roles in modulating breast cancer immunobiology. Collectively, this study elucidates the therapeutic potential of YW-LF, a ribociclib derivative, in breast cancer treatment and delineates its multifaceted mechanisms, offering a promising strategy to overcome the limitations of current CDK4/6 inhibitors.

2025-04-11 | GSE294223 | GEO

Ribociclib Derivative RB-BC Induces Apoptosis in Breast Cancer through p53 Pathway Activation

Project description:Ribociclib Derivative RB-BC Induces Apoptosis in Breast Cancer through p53 Pathway Activation

| PRJNA1250294 | ENA

Novel Ribociclib Derivative RB-1 Exhibits Anti-breast Cancer Actions by Regulating p53 and Cell Cycle Pathways

Project description:Breast cancer remains the most prevalent malignancy among women globally, with its incidence continuing to rise and ranking as the leading cause of cancer-related mortality in females. Ribociclib, a cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor, suppresses tumor cell proliferation by blocking the transition from the G1 to S phase. This study investigates the molecular mechanisms and therapeutic efficacy of RB-1 (7-cyclopentyl-N-ethyl-N-methyl-2-((3-(4-methyl-1H-imidazol-1-yl)-5-(trifluoromethyl)phenyl)amino)-7H-pyrrolo[2,3-d]pyrimidine-6-carboxamide), a novel Ribociclib derivative, in inhibiting breast cancer progression. The effects of RB-1 on breast cancer cell viability were evaluated via MTT assay. In vitro and in vivo experiments demonstrated that RB-1 significantly inhibited cell proliferation, colony formation, and the proportion of EdU-positive cells in multiple breast cancer cell lines (e.g., MDA-MB-231 and SKBR3). The chicken chorioallantoic membrane (CAM) assay revealed that RB-1 treatment markedly suppressed tumor angiogenesis, outperforming Ribociclib. Mechanistic studies indicated that RB-1 regulates the p53 signaling pathway and cell cycle-related targets (e.g., E2F targets, mitotic spindle assembly), specifically inhibiting CDK4/6-mediated cell cycle progression. Furthermore, machine learning analysis identified Hyaluronan-Mediated Motility Receptor (HMMR) as a diagnostic and prognostic biomarker for breast cancer, with its expression significantly correlating with tumor-infiltrating immune cells. This study highlights the anti-cancer potential of RB-1 and elucidates its molecular mechanisms, offering a promising therapeutic candidate and novel targets for breast cancer treatment.

2025-04-12 | GSE294375 | GEO

Transcriptional profiling of ribociclib-treated sensitive and ribociclib resistant CAMA-1 cells

Project description:We report transcriptional response to ribociclib treatment in resistant and sensitive CAMA-1 cells using RNA sequencing. Acquired ribociclib resistant cells were generated by treating CAMA-1 cells over a period of 5 month. Cells were then treated with ribociclib or DMSO control and processed for RNA sequencing.

2020-06-22 | GSE143944 | GEO

ChIP-seq data from fkh-Gal4::UAS-rib-GFP and sage-Gal4::UAS-rib-GFP mid- through late-stage Drosophila embryos

Project description:Transcription factors, which regulate the spatiotemporal patterns of gene expression during organogenesis, often regulate multiple aspects of tissue morphogenesis, including cell-type specification, cell proliferation, cell death, cell polarity, cell shape, cell arrangement and cell migration. In this work, we describe a distinct role for Ribbon (Rib) in controlling cell shape changes during elongation of the Drosophila salivary gland (SG). Notably, the morphogenetic changes in rib mutants occurred without effects on general SG cell attributes such as specification, proliferation and apoptosis. Moreover, the abnormal cell/organ shape in rib mutants occurred without compromising epithelial-specific morphological attributes such as apicobasal polarity and junctional integrity. To identify the genes regulated by Rib that control cell and organ shape, we performed ChIP-seq analysis in embryos driving rib expression specifically in the SGs. To learn if the Rib binding sites identified in the ChIP-seq analysis were linked to changes in gene expression through transcriptional activation, repression, or both, we performed microarray analysis comparing RNA samples from age-matched wild-type and rib null embryos. From the superposed ChIP-seq and microarray gene expression data, we identified 60 genomic sites of bound Rib most likely to regulate SG-specific gene expression. We confirmed several of the identified Rib targets by qRT-pCR and/or in situ hybridization. Our results indicate that Rib regulates cell shape change in the Drosophila salivary gland via a diverse array of targets through both transcriptional activation and repression. Furthermore, our results suggest that a critical component of the SG morphogenetic gene network involving Rib is its autoregulation.

2015-12-21 | GSE73780 | GEO

A novel Ribociclib derivative, YW-LF, exerts anti-breast cancer effects by activating the p53 pathway.

Project description:A novel Ribociclib derivative, YW-LF, exerts anti-breast cancer effects by activating the p53 pathway.

| PRJNA1248763 | ENA

Effect of ribociclib on breast cancer cells

Project description:To study mechanisms underlying response to ribociclib.

2022-01-10 | GSE182288 | GEO

Novel Ribociclib Derivative RB-1 Exhibits Anti-breast Cancer Actions by Regulating p53 and Cell Cycle Pathways

Project description:Novel Ribociclib Derivative RB-1 Exhibits Anti-breast Cancer Actions by Regulating p53 and Cell Cycle Pathways

| PRJNA1249285 | ENA