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CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [SNU308]

ABSTRACT: CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [SNU308]

PROVIDER: PRJNA1017683 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26068942_1.fastq.gz	Fastqsanger.gz
	SRR26068942_2.fastq.gz	Fastqsanger.gz
	SRR26068943_1.fastq.gz	Fastqsanger.gz
	SRR26068943_2.fastq.gz	Fastqsanger.gz
	SRR26068944_1.fastq.gz	Fastqsanger.gz

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CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [SNU308]

Project description:Gallbladder cancer (GBC) comprises the most common biliary tract cancer (BTC). However, GBC is a rare disease often manifesting as aggressive malignancy due to its late diagnosis and resistance to chemotherapy. The identification of molecular drivers of GBC and identification of targeted therapies is still urgently needed. This study combined proteomic analysis of GBC patient samples, functional and molecular characterization of potential oncogenes, and identification of potential therapy strategy for GBC. We identified Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) as one of the strongest and most significant upregulated proteins in GBC samples. Functional analysis and in vivo mouse models revealed that CEACAM6 supported the initial steps of cancer metastasis by decreasing cell adhesion while promoting migration and invasion of GBC cells. BirA-BioID followed by mass-spectrometry revealed Integrin Beta-1 (ITGB1) and Protein Kinase C Delta (PRKCD) as direct molecular and functional partners of CEACAM6 in supporting GBC cell migration through regulation of ERK and AKT downstream target genes MMP13, MMP14, and OCLN. Conversely, CEACAM6 knockdown abolished GBC aggressiveness, and treatment using AKT inhibitor Capivasertib and ERK inhibitor Ulixertinib counter-acted the CEACAM6-induced migration.These findings demonstrate that CEACAM6 is crucial for gallbladder oncogenesis through ERK and AKT signaling, providing insights into the design of therapeutic strategies for GBC.

2024-10-30 | GSE243304 | GEO

CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [GB-d1]

2024-10-30 | GSE243305 | GEO

CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD.

Project description:CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD.

| PRJNA1017681 | ENA

CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [GB-d1]

Project description:CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD [GB-d1]

| PRJNA1017684 | ENA

CEACAM6 orchestrates gallbladder cancer aggressiveness through molecular interplay with Integrin and PRKCD.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-10-30 | GSE243306 | GEO

Effects of siRNA targeting PRKCD in breast cancer cells

Project description:The aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines. MDA-MB-468 and BT-549 breast cancer cell lines were treated with control siRNA or siRNA targeting PRKCD. Three samples in each group were analyzed.

2015-03-01 | E-GEOD-55503 | biostudies-arrayexpress

Macrophage migration inhibitory factor - a therapeutic target in gallbladder cancer

Project description:Poor prognosis in gallbladder cancer is due to late presentation of the disease, lack of reliable biomarkers for early diagnosis and limited targeted therapies. Early diagnostic markers and novel therapeutic targets can significantly improve clinical management of GBC. We carried out quantitative proteomic analysis using a panel of gallbladder cancer cell lines using isobaric tags for relative and absolute quantitation (iTRAQ). We identified 3,655 proteins among which 654 were found to be overexpressed and 387 were downregulated in the invasive cell lines (OCUG-1, NOZ and GB-d1) compared to the non-invasive cell line, TGBC24TKB. Among these, macrophage inhibitory factor (MIF) was observed to be >3-fold overexpressed. MIF is a pleiotropic proinflammatory cytokine that plays a causative role in multiple diseases including cancer. MIF has been reported to play a central role in tumor cell proliferation and invasion in several cancers. Immunohistochemical staining confirmed our findings showing overexpression of MIF in 21 of 29 gallbladder adenocarcinoma cases. A significant decrease in cell viability, colony forming ability and invasive property of the gallbladder cancer cells was observed upon MIF inhibition using MIF siRNA and MIF antagonists. Our findings support the role of MIF in tumor aggressiveness and suggest its potential application as a therapeutic target for gallbladder cancer.

2015-10-02 | PXD001566 | Pride

Effects of siRNA targeting PRKCD in breast cancer cells

Project description:The aim was to identify genes that were commonly influenced by a siRNA targeting PRKCD in breast cancer cell lines.

2015-03-01 | GSE55503 | GEO

microRNAseq of primary human gallbladder cells, reprogrammed human gallbladder cells, and human pancreatic beta cells

Project description:We determined the global microRNA expression profiles of primary human gallbladder cells and genetically reprogrammed human gallbladder cells and compared with pancreatic beta cells to ascertain the degree of cellular transdifferentatiation of insulin-producing human gallbladder cells to become beta-like cells. First, we cultured patient-derived gallbladder cells and then we transduced these with beta cell transcription factors to reprogram gallbladder cells to become beta-like cells. We used a pan-islet surface monoclonal antibody to enrich for insulin-producing reprogrammed human gallbladder cells using FACS.

2017-08-02 | E-MTAB-5554 | biostudies-arrayexpress

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Project description:We determined the global gene expression profiles of primary human gallbladder cells and genetically reprogrammed human gallbladder cells and compared with pancreatic beta cells to ascertain the degree of cellular transdifferentatiation of insulin-producing human gallbladder cells to become beta-like cells. First, we cultured patient-derived gallbladder cells and then we transduced these with beta cell transcription factors to reprogram gallbladder cells to become beta-like cells. We used a pan-islet surface monoclonal antibody to enrich for insulin-producing reprogrammed human gallbladder cells using FACS.

2017-08-02 | E-MTAB-5556 | biostudies-arrayexpress

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