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New strategy for breast cancer treatment: Neoribocic inhibits tumor proliferation through cell cycle blockade

ABSTRACT: New strategy for breast cancer treatment: Neoribocic inhibits tumor proliferation through cell cycle blockade

PROVIDER: PRJNA1249459 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33082296_1.fastq.gz	Fastqsanger.gz
	SRR33082296_2.fastq.gz	Fastqsanger.gz
	SRR33082297_1.fastq.gz	Fastqsanger.gz
	SRR33082297_2.fastq.gz	Fastqsanger.gz
	SRR33082298_1.fastq.gz	Fastqsanger.gz

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Project description:As one of the most common malignant tumors in the world, breast cancer is still a major challenge to human health despite the continuous improvement of treatment methods. Therefore, it is of great clinical significance to develop new anti-breast cancer drugs to improve the therapeutic effect. As a CDK4/6 inhibitor, Ribociclib has shown potential in breast cancer treatment. Based on this, we designed and synthesized a new type of ribocyclib derivative Neoribocic, and deeply studied its role mechanism in breast cancer. Research results show that Neoribocic can significantly inhibit the proliferation, migration and invasion ability of breast cancer cells in in vitro experiments, and show excellent anti-tumor activity. By analyzing MDA-MB-231 cells treated with Neoribocic through RNA sequencing (RNA-Seq), we found that Neoribocic may block the progression of breast cancer cells in the G2/M stage by activating the p53 signaling pathway, thus exerting their anti-tumor effect. . In addition, in vivo experiments further confirm that Neoribocic can not only effectively inhibit tumor growth, but also significantly inhibit the angiogenesis in the chicken embryonic cyst membrane, suggesting that it may have an anti-angiogenesis effect.

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OTX2 drives medulloblastoma proliferation via direct regulation of cell cycle genes and inhibits differentiation

Project description:The transcription factor OTX2 has been implicated as an oncogene in medulloblastoma, which is the most common malignant brain tumor in children. It is highly expressed in most medulloblastomas and amplified in a subset of them. The role of OTX2 in medulloblastoma and its downstream targets are unclear. Therefore, we generated D425 medulloblastoma cells in which we can silence endogenous OTX2 by inducible shRNA. Silencing of OTX2 strongly inhibited cell proliferation and resulted in a neuronal-like differentiation. Expression profiling of time courses after silencing showed a progressive change in gene expression for many cellular processes. Down regulated genes were highly enriched for cell cycle and visual perception genes, while up regulated genes were enriched for genes involved in development and differentiation. This shift in expression profiles is reminiscent to changes described to occur during normal cerebellum development. OTX2 is expressed in proliferating granular progenitor cells, but the expression diminishes when these cells exit the cell cycle and start differentiating. ChIP-on-chip analyses of OTX2 in D425 cells showed that cell cycle and perception genes were direct OTX2 targets, while regulation of most differentiation genes appears to be indirect. These analyses provide the first insight in the molecular network of OTX2, demonstrating that OTX2 is essential in medulloblastoma and directly drives proliferation by regulating the expression of cell cycle genes. Since many of these genes also correlate in expression with OTX2 in primary tumors, they might be potential targets for therapy in medulloblastoma patients. Keywords: OTX2, medulloblastoma, mRNA profiling *** This Series represents the gene expression component of the study. Three independent time course experiments of OTX2 silencing, and 1 control experiment in D425 medulloblastoma cells.

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