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Effect of knockdown of GRP94 on gene expression of MKN-45 cells

ABSTRACT: Effect of knockdown of GRP94 on gene expression of MKN-45 cells

PROVIDER: PRJNA1113161 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29076629_1.fastq.gz	Fastqsanger.gz
	SRR29076629_2.fastq.gz	Fastqsanger.gz
	SRR29076630_1.fastq.gz	Fastqsanger.gz
	SRR29076630_2.fastq.gz	Fastqsanger.gz
	SRR29076631_1.fastq.gz	Fastqsanger.gz

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Effect of knockdown of GRP94 on gene expression of MKN-45 cells

Project description:Anoikis resistance allows cancer cells to avoid death caused by detachment from the extracellular matrix's adhesion, enabling these cells to infiltrate and migrate to regions such as the peritoneum.Glucose-regulated protein 94 (GRP94, alternatively labeled as HSP90B1) is typically stress-induced and is part of the heat shock protein 90 (Hsp90) family.GRP94 is closely tied to cellular resistance to stress, apoptosis, proliferation, invasion, inflammation, and immunity.Our findings indicated that while attached culture didn't impact the apoptosis rate between shGRP94 and shCtrl groups, GRP94 knockdown weakened anoikis resistance, migration, and invasion abilities. Here, we aim to assess the impact of knocking down GRP94 on gene expression in the gastric cancer cell line MKN-45, to further elucidate potential molecular mechanisms by which GRP94 affects the biological characteristics of gastric cancer cells.

2024-07-25 | GSE267811 | GEO

Genome-wide maps in gastric cancer MKN-45 cells with or without the overexpression of transcriptional factor SIX2

Project description:Analysis of MKN-45 cells following SIX2 stable overexpression or not. SIX2 regulates various mRNA expression in MKN-45 cells.Results provide insight into the role of SIX2-involved mechanisms underlying SIX2-mediated effects on gastric cancer stemness.

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microarray Analysis of MKN-45 cell lines after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.

Project description:We demonstrate that miR-125b, a key node in this microRNA regulatory network, is upregulated in gastric cancer (GC) and associated with poor overall survival through an integrated analysis of microRNA and mRNA profiling of GC revealed a mRNA-regulatory network.So we have employed whole genome microarray expression profiling as a discovery platform to compare the transcriptome profiling of human gastric cells (MKN-45) after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.Pathway analysis shows that the predicted targets of miR-125b are highly involved in apoptosis/program death pathway，and the robust apoptosis genes, BIK and CASP6 are validated as the directed targets of miR-125b.

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Gene expression profiling data following PTBP1 knockout in MKN-28 cells

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Effect of TUC338 knockdown on gene expression

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Transcriptome analysis of highly metastatic cell line

Project description:A prediction of peritoneal recurrence is of significance using metastasis-related biomarker. This work describes a combined analysis of proteome and transcriptome data for biomarker discovery in highly metastatic cell line. We used nano-flow liquid chromatography (LC) linear ion trap time-of-flight mass spectrometry (LIT-TOF MS) and cDNA microarray to identify specific protein differentially expressed between a highly metastatic stomach cancer cell line MKN-45-P and its parental cell line MKN-45. In total, 240 proteins were found to be expressed between the two cell lines. Of these, 75 proteins (31%) and 49 proteins (20%) were only identified from MKN-45-P and MKN-45 respectively. An mRNA expression of 1533 genes was up-regulated in MKN-45-P compared with MKN-45. No close correlation was found between proteomic and transcriptomic analysis. Interestingly, 4 of 240 proteins (1.6%) were involved in the up-regulated mRNA expression. Comparison analysis of gene expression between highly metastatic gastric cancer cell line MKN-45-P and its parental cell line MKN-45.

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TASK-3 Gene Knockdown Dampens Invasion and Migration and Promotes Apoptosis in KATO III and MKN-45 Human Gastric Adenocarcinoma Cell Lines.

Project description:Incidence and mortality of gastric cancer is increasing worldwide, in part, because of the lack of new therapeutic targets to treat this disease. Different types of ion channels participate in the hallmarks of cancer. In this context, ion channels are known to exert control over the cell cycle, mechanisms that support survival, angiogenesis, migration, and cell invasion. In particular, TASK-3 (KCNK9), a member of the K2P potassium channel family, has attracted much interest because of its oncogenic properties. However, despite multiple lines of evidence linking TASK-3 to tumorigenesis in various types of cancer, its relationship with gastric cancer has not been fully examined. Therefore, we set out to assess the effect of TASK-3 gene knockdown on KATO III and MKN-45 human gastric adenocarcinoma cell lines by using a short hairpin RNA (shRNA)-mediated knockdown. Our results demonstrate that knocking down TASK-3 reduces cell proliferation and viability because of an increase in apoptosis without an apparent effect on cell cycle checkpoints. In addition, cell migration and invasion are reduced after knocking down TASK-3 in these cell lines. The present study highlights TASK-3 as a key protein involved in migration and cell survival in gastric cancer and corroborates its potential as a therapeutic target for gastric cancer treatment.

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