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The role of MSK1 in pancreatic adenocarcinoma (PDAC) progression

ABSTRACT: The role of MSK1 in pancreatic adenocarcinoma (PDAC) progression

PROVIDER: PRJNA631533 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11746760.fastq.gz	Fastqsanger.gz
	SRR11746761.fastq.gz	Fastqsanger.gz
	SRR11746762.fastq.gz	Fastqsanger.gz
	SRR11746763.fastq.gz	Fastqsanger.gz
	SRR11746764.fastq.gz	Fastqsanger.gz

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The role of KLF7 in pancreatic adenocarcinoma (PDAC) progression

Project description:The role of KLF7 in pancreatic adenocarcinoma (PDAC) progression

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HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway via stimulating MSK1 kinase and suppressing PPP2R2B protein

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective therapies. We demonstrated that the transcription factor, HOXC6, was overexpressed in most PDACs, and its inhibition blocked PDAC tumor growth and metastasis. HOXC6 transcriptionally activated the tumor-promoting kinase MSK1. To identify the phosphorylation targets of MSK1 and the mediators of its function in PANC1 cells, we utilized an unbiased TMT10-based phosphoproteomics analysis. To do so, we treated AsPC1 cells with MSK1 inhibitor SB-747651A and performed TMT10-based quantitative phosphoproteomics analysis and identified MSK1 phosphorylation targets.

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HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway via stimulating MSK1 kinase and suppressing PPP2R2B protein

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective therapies. We demonstrated that the transcription factor, HOXC6, was overexpressed in most PDACs, and its inhibition blocked PDAC tumor growth and metastasis. HOXC6 transcriptionally activated the tumor-promoting kinase MSK1. To identify the phosphorylation targets of MSK1 and the mediators of its function in AsPC1 cells, we utilized an unbiased TMT10-based phosphoproteomics analysis. To do so, we treated AsPC1 cells with MSK1 inhibitor SB-747651A and performed TMT10-based quantitative phosphoproteomics analysis and identified MSK1 phosphorylation targets.

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HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway via stimulating MSK1 kinase and suppressing PPP2R2B protein

Project description:Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers, which lacks effective therapies. Here, we demonstrate that the transcription factor, HOXC6, is overexpressed in most PDACs, and its inhibition blocks PDAC tumor growth and metastasis. HOXC6 transcriptionally activates tumor-promoting kinase MSK1 and suppresses tumor-inhibitory protein PPP2R2B in PDAC. HOXC6-induced PPP2R2B suppression causes mTOR pathway activation, which facilitates PDAC growth. Also, MSK1 upregulation by HOXC6 is necessary for PDAC growth due to its ability to suppress apoptosis via its substrate DDX17. Combinatorial pharmacological inhibition of MSK1 and mTOR potently suppressed PDAC tumor growth and metastasis in PDAC mouse models. PDAC cells with acquired resistance to MSK1/mTOR-inhibitors displayed activated IGF1R signaling and were successfully eradicated by IGF1R inhibitor. Furthermore, MEK inhibitor trametinib enhanced the efficacy of dual MSK1 and mTOR inhibition. Collectively, these results identify therapeutic vulnerabilities of PDAC and an approach to overcome acquired drug resistance to prolong therapeutic benefit.

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HOXC6 drives a therapeutically targetable pancreatic cancer growth and metastasis pathway via stimulating MSK1 kinase and suppressing PPP2R2B protein

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