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RNA-seq of H1299 cells in which either PRKCI or SOX2 was silenced by validated lentiviral shRNA constructs

ABSTRACT: RNA-seq of H1299 cells in which either PRKCI or SOX2 was silenced by validated lentiviral shRNA constructs

PROVIDER: PRJNA594340 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10611700_1.fastq.gz	Fastqsanger.gz
	SRR10611700_2.fastq.gz	Fastqsanger.gz
	SRR10611701_1.fastq.gz	Fastqsanger.gz
	SRR10611701_2.fastq.gz	Fastqsanger.gz
	SRR10611702_1.fastq.gz	Fastqsanger.gz

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RNA-seq of H1299 cells in which either PRKCI or SOX2 was silenced by validated lentiviral shRNA constructs

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PRKCI regulates tumor microenvironment through YAP1 [Affymetrix]

Project description:A key feature of serous ovarian cancer is frequent amplification in the 3q26 locus, which harbors the PRKCI gene. Here we show that PRKCI is amplified and overexpressed in a 78% of high-grade serous ovarian carcinoma. Our in vivo studies with orthotopic mouse models establish it as an ovarian cancer oncogene. This oncogenic property of PRKCI is mediated by regulation of YAP1 activity. Accordingly YAP1 knockdown partially rescues PRKCI mediated tumorigenesis. Integrated gene expression profiling and YAP1 promoter occupancy analyses reveal that PRKCI and YAP1 cooperate to transcriptionally regulate genes affecting the tumor immune microenvironment. Consistently, CD11b+Gr1+Ly6G+ MDSCs are increased in the tumor microenvironment of PRKCI over-expressing tumors. Importantly, we show that elevated PRKCI expression in high-grade serous ovarian carcinomas strongly correlated with assignment to immunoreactive subtype. In summary, we identify PRKCI and YAP1 as key mediators of a tumor-promoting immunosuppressive microenvironment in ovarian cancers.

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Project description:A key feature of ovarian high-grade serous carcinoma is frequent amplification of the 3q26 locus. Here we show that PRKCI, located on the 3q26 locus is not only amplified and overexpressed in 78% of HGSC patient samples but is also expressed in early fallopian tube lesions, called Serous Tubal Intraepithelial Carcinoma. In vivo studies in a transgenic mouse model establish PRKCI as an ovarian cancer oncogene and identify YAP1 as a downstream regulator. Together, PRKCI and YAP1 regulate TNFα to promote an immune suppressive microenvironment and inhibit cytotoxic T-cell infiltration in tumors. High PRKCI expressing human ovarian tumors show decreased cytotoxic T-cell infiltration. Taken together, we identify PRKCI and YAP1 as key mediators of a tumor-promoting immune microenvironment in ovarian cancer.

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