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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.

2023-12-08 | GSE228690 | GEO

Effect of knocking down HOXB9 in gastric cancer cells

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Effect of knocking down FOXP4 and YAP1 in gastric cancer cells

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Effect of stimulating 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. As Yoda1 is known to be an agonist of PIEZO1, we try to explore the PIEZO1 function in GC by Yoda1 treatment.

2023-12-08 | GSE228691 | GEO

Effect of stimulating PIEZO1 in gastric cancer cells

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Effect of knocking down HOXB9 in gastric cancer cells

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.

2023-01-31 | GSE223763 | GEO

Effect of knocking down FOXP4 and YAP1 in gastric cancer cells

Project description:The Hippo-YAP1 pathway is an evolutionally conserved signaling cascade that controls organ size and tissue regeneration. Its dysregulation has been well-studied to promote tumor initiation and progression, including gastric cancer (GC). Although the Hippo-YAP1 signaling pathway regulates the expression of thousands of target genes, how these target genes contribute to the oncogenic program driven by YAP1 remains unknown. Here we identified the vital role of FOXP4 in YAP1-driven gastric carcinogenesis by maintaining stemness and promoting peritoneal metastasis. Knocking down FOXP4 impairs GC spheroid formation and inhibits stemness marker expression, while its upregulation potentiates the cancer cells with more stemness. RNA-seq analysis revealed SOX12 as functional downstream of FOXP4 in the YAP1-induced carcinogenesis. Targeting FOXP4 by 42-(2-Tetrazolyl) rapamycin in GC cells enhanced the 5-FU efficacies. Our findings have unveiled FOXP4 as a novel stemness marker that promotes tumorigenesis by upregulating SOX12. Additionally, we have identified FOXP4 as a direct target for modulating YAP1 signaling in GC. Therefore, the YAP1-FOXP4-SOX12 axis presents a promising therapeutic target for GC.

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Expression data from control and GAPLINC knock down human gastric cancer cell lines

Project description:Transcriptional profiling of comparing control and GAPLINC stable knocking-down human gastric cancer cell lines. Goal was to determine the different gene expression between control and GAPLINC stable knocking-down human gastric cancer cell lines. Control and GAPLINC stable knocking-down human gastric cancer cell lines were prepared for RNA extraction and hybridization on Affymetrix microarrays.

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