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Transcriptome of yw fly, L(3)mbt mutant fly and Lint-O mutant fly were performed in triplicate in Drosophila melanogaster

ABSTRACT: Transcriptome of yw fly, L(3)mbt mutant fly and Lint-O mutant fly were performed in triplicate in Drosophila melanogaster

PROVIDER: PRJNA846302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19546800_1.fastq.gz	Fastqsanger.gz
	SRR19546800_2.fastq.gz	Fastqsanger.gz
	SRR19546801_1.fastq.gz	Fastqsanger.gz
	SRR19546801_2.fastq.gz	Fastqsanger.gz
	SRR19546802_1.fastq.gz	Fastqsanger.gz

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Transcriptome of yw fly, L(3)mbt mutant fly and Lint-O mutant fly were performed in triplicate in Drosophila melanogaster

Project description:L(3)mbt regulates the transcription of germ-specific genes in somatic cells but the detailed mechanism remains unclear. We performed ChIP-seq of L(3)mbt and a newly identified interactor in OSCs to elucidate the genome-wide localization. Then we performed RNA-seq of OSCs before and after RNAi treatment of L(3)mbt and its interactors and performed differential expression analysis.

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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.

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