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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 data of H1299 from NT versus PRKCI KD and NT versus SOX2 KD cells. Analysis revealed activation of oncogenic signaling pathways by PRKCI and SOX2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE141666 | GEO | 2019/12/10

REPOSITORIES: GEO

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

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

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RNA-seq of Tumor Initiating Cells (TICs) from Lung Squamous Cell Carcinoma (LSCC) lines reveals PRKCI dependent Hedgehog (HH) Signalling

Project description:RNA-seq analysis was performed on TICs and the parental counterparts of 4 LSCC cell lines. In addition, PRKCI knock down (KD) variants of these cells were sequenced. Subsequent analysis revealed that activation of HH signaling, a known driver of the TIC phenotype, is dependent on PRKCI expression. Examination of TICS, parental cells, parental PRKCI KD cells, and TIC PRKCI KD cells

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RNA-seq of Tumor Initiating Cells (TICs) from Lung Squamous Cell Carcinoma (LSCC) lines reveals PRKCI dependent Hedgehog (HH) Signalling

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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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PRKCI promotes immune suppression in ovarian cancer through YAP1

Project description:A key feature of high-grade serous ovarian carcinoma (HGSOC) is frequent amplification of the 3q26 locus harboring PRKC-iota (PRKCI). Here, we show that PRKCI is also expressed in early fallopian tube lesions, called Serous Tubal Intraepithelial Carcinoma. Transgenic mouse studies establish PRKCI as an ovarian cancer specific oncogene and system level and functional analyses identify YAP1 as a downstream effector in tumor progression. Mechanistically, the oncogenic activity of the PRKCI-YAP1 axis relates in part to the upregulation of TNFα to promote an immune suppressive tumor microenvironment characterized by an abundance of myeloid-derived suppressor cells and inhibition of cytotoxic T cell infiltration. In human ovarian cancers, high PRKCI expression also correlates with high expression of YAP1 and low infiltration of cytotoxic T-cell. The PRKCI-YAP1 regulation of the tumor immunity provides a therapeutic strategy for highly lethal ovarian cancer. Robust multi-array average (RMA) method was used with default options (with background correction, quantile normalization, and log transformation) to normalize raw data from batches using R/Bioconductor‘s affy package

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Gene Expression Profiling in PRKCI vs NT-silenced Cells

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PRKCI regulates tumor microenvironment through YAP1

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