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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

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2022-07-22 | PXD035125 | Pride

RNAseq of parental and neratinib resistant 5637 and OVCAR8 cells with or withour neratinib treatment

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Sinorhizobium meliloti strain:7A

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RNAseq of parental and neratinib resistant 5637 and OVCAR8 cells with or withour neratinib treatment

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Metabolic reprogramming of triple-negative breast cancer and melanoma cell lines by the Let-7a microRNA

Project description:Let-7 microRNAs (miRNAs) are a family of highly conserved well-established promoters of terminal differentiation that are expressed in all healthy adult tissues and frequently repressed in cancer cells. The tumour suppressive role of let-7 in a variety of cancers in vitro and in vivo has been widely documented and prompted these miRNAs to be candidate genes for miRNA replacement therapy. Reprogrammed metabolism, recently identified as a new hallmark of cancer, contributes to cancer cell growth, proliferation, invasiveness and drug resistance. In this study we identified a new metabolic role of let-7a in triple-negative breast cancer and metastatic melanoma cell lines. We show that let-7a down-regulates key anabolic enzymes, promotes oxidative phosphorylation and mitochondrial ROS formation accompanied by the up-regulation of the oxidative stress responsive genes. To assess if we could exploit these increased ROS levels for therapeutic purposes, we combined let-7a transfection with the antitumor drug doxorubicin. In both cancer types we observed a stronger response to the doxorubicin treatment in let-7a transfected cells. Pre-treatment with an antioxidant N-acetyl cysteine totally abolished this difference, indicating that the increased doxorubicin sensitivity of let-7a cells depends on the redox pathway. We demonstrated that let-7a plays a prominent role in regulating energy metabolism in cancer cells. We propose that a benefit from let-7 miRNA replacement therapy could come not only from the repression of oncogenic pathways targeted directly by let-7, but also by increased sensitivity to chemotherapeutic agents through indirect metabolic changes caused by let-7. Investigation of let-7a metabolic role in breast cancer and melanoma cells.

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