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Neratinib derivative 7A induces apoptosis in colon cancer cells via the p53 pathway

ABSTRACT: Neratinib derivative 7A induces apoptosis in colon cancer cells via the p53 pathway

PROVIDER: PRJNA1176976 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31096287_1.fastq.gz	Fastqsanger.gz
	SRR31096287_2.fastq.gz	Fastqsanger.gz
	SRR31096288_1.fastq.gz	Fastqsanger.gz
	SRR31096288_2.fastq.gz	Fastqsanger.gz
	SRR31096289_1.fastq.gz	Fastqsanger.gz

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Neratinib derivative 7A induces apoptosis in colon cancer cells via the p53 pathway

Project description:Colorectal cancer remains a significant health threat, with its incidence continuously rising, underscoring the urgent need for the development of new therapeutic agents. In our previous research, we identified 7A, a derivative of Neratinib, as having pronounced antitumor activity. However, its specific effects and mechanisms in colorectal cancer have not been thoroughly investigated. Therefore, this study employed in vivo and in vitro experiments, utilizing techniques such as RNA sequencing, Western blotting, and PCR, to provide a comprehensive analysis of 7A's mechanism of action in colorectal cancer. The results indicate that 7A induces DNA damage and activates the P53 pathway, thereby promoting apoptosis in colorectal cancer cells. Additionally, 7A treatment significantly reduced angiogenesis and tumor weight. Our findings suggest that 7A, a Neratinib derivative, holds promise as a novel candidate for colorectal cancer therapy.

2024-11-02 | GSE280188 | GEO

¬The EGFR/ErbB inhibitor neratinib promotes apoptosis and clearance by airway macrophages

Project description:Dysregulated neutrophilic inflammation can be highly destructive in chronic inflammatory diseases due to prolonged neutrophil lifespan and continual release of histotoxic mediators in inflamed tissues. Inducing neutrophil apoptosis, an immunologically silent form of cell death, may be beneficial in these diseases, provided that the apoptotic neutrophils are efficiently cleared from the tissue. Our previous research identified ErbB inhibitors as able to induce neutrophil apoptosis and reduce neutrophilic inflammation both in vitro and in vivo (Rahman et al. 2019). Here we expand on that work using a clinical ErbB inhibitor, neratinib, which has the potential to be repurposed in inflammatory diseases. We show that neratinib reduces neutrophilic migration to an inflammatory site in zebrafish larvae. Neratinib upregulates efferocytosis and reduces the number of dead neutrophils in mouse models of acute, but not chronic, lung injury, suggesting the drug may have therapeutic benefits in acute inflammatory settings. Phosphoproteomics analysis of human neutrophils shows that neratinib modifies the phosphorylation of proteins regulating apoptosis, migration and efferocytosis. This work identifies a potential efficacious mechanism for neratinib in acute lung inflammation by upregulating the clearance of dead neutrophils, and examination of the neutrophil phosphoproteome gives insight into the mechanisms by which this may be occurring.

2022-07-22 | PXD035125 | Pride

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

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

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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

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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.

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