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Effect of knocking down PIEZO1 in gastric cancer cells

ABSTRACT: Effect of knocking down PIEZO1 in gastric cancer cells

PROVIDER: PRJNA951218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24039365_1.fastq.gz	Fastqsanger.gz
	SRR24039365_2.fastq.gz	Fastqsanger.gz
	SRR24039366_1.fastq.gz	Fastqsanger.gz
	SRR24039366_2.fastq.gz	Fastqsanger.gz

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Effect of knocking down PIEZO1 in gastric cancer cells

Project description:In gastric cancer (GC), PIEZO1 was suggested to promote cell migration by interacting with Trefoil factor family 1 (TFF1) and serve as a therapeutic target against invasion and metastasis. In addition, PIEZO1 demonstrates abundant expression in most GC cell lines and primary samples and highly-expressed PIEZO1 is associated with poor disease-specific survival. Thus, we try to explore the PIEZO1 function in GC by knocking down assay.

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Project description:HOX proteins play fundamental roles during ontogenesis by interacting with other non-HOX gene-encoded partners and performing transcriptional functions, while aberrant activation of HOX members drives tumorigenesis. In this study, gastric cancer (GC) expression microarray data indicates that HOXB9 is a prominent upregulated HOX member in GC samples and is significantly associated with clinical outcomes and advanced TNM stages. However, the functional role of HOXB9 in GC remains contradictory in previous reports, and the regulatory mechanisms are elusive. By in silico and experimental analyses, we found HOXB9 was upregulated by a vital cell cycle-related transcription factor E2F1. Depleting HOXB9 causes G1 phase cell cycle arrest by downregulating CDK6 and a subset of cell cycle-related genes. Meanwhile, HOXB9 contributes to cell division and maintains the cytoskeleton in GC cells. PBX2 is a potential transcription factor for CDK6. We verified that HOXB9 interacts with PBX2 to form a heterodimer and upregulates CDK6. Knocking down CDK6 can phenocopy the tumor-suppressive effects of HOXB9 depletion. Inhibiting HOXB9 can enhance the anti-tumor effect of CDK6 inhibitors on GC growth. In conclusion, we elucidate the oncogenic role of HOXB9 and reveal CDK6 as its potent downstream modulator in GC.

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