Name: Phosphoproteomics of PDT treated SK-ChA-1 cells
Keywords: Pdt

Dataset Information

Phosphoproteomics of PDT treated SK-ChA-1 cells

ABSTRACT: (Phospho)proteomic study of the cell survival pathways induced by ZnPC-encapsulating PEGylated cationic liposomes (ZPCLs) in SK-ChA-1 cells.

OTHER RELATED OMICS DATASETS IN: GSE84758PRJNA331051PRJNA331048PRJNA331050

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Simone Lemeer

LAB HEAD: Simone Lemeer

PROVIDER: PXD004320 | Pride | 2018-10-27

REPOSITORIES: Pride

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Publications

Multi-OMIC profiling of survival and metabolic signaling networks in cells subjected to photodynamic therapy.

Weijer Ruud R Clavier Séverine S Zaal Esther A EA Pijls Maud M E MM van Kooten Robert T RT Vermaas Klaas K Leen René R Jongejan Aldo A Moerland Perry D PD van Kampen Antoine H C AH van Kuilenburg André B P AB Berkers Celia R CR Lemeer Simone S Heger Michal M

Cellular and molecular life sciences : CMLS 20161101 6

Photodynamic therapy (PDT) is an established palliative treatment for perihilar cholangiocarcinoma that is clinically promising. However, tumors tend to regrow after PDT, which may result from the PDT-induced activation of survival pathways in sublethally afflicted tumor cells. In this study, tumor-comprising cells (i.e., vascular endothelial cells, macrophages, perihilar cholangiocarcinoma cells, and EGFR-overexpressing epidermoid cancer cells) were treated with the photosensitizer zinc phthalo ...[more]

PMID: 27803950

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Project description:Photodynamic therapy (PDT) of solid cancers comprises the administration of a photosensitizer followed by illumination of the photosensitizerreplete tumor with laser light. This induces a state of local oxidative stress, culminating in the destruction of tumor tissue and microvasculature and induction of an anti-tumor immune response. However, some tumor types, including perihilar cholangiocarcinoma, are relatively refractory to PDT, which may be attributable to the activation of survival pathways in tumor cells following PDT (i.e., activator protein 1 (AP-1)-, nuclear factor of kappa light polypeptide gene enhancer in B-cells (NF-ÎºB)-, hypoxia-inducible factor 1-alpha (HIF-1Î±)-, nuclear factor (erythroid-derived 2)-like 2 (NFE2L2), and unfolded protein response-mediated pathways). To assess the activation of survival pathways after PDT, human perihilar cholangiocarcinoma (SK-ChA-1) cells were subjected to PDT with zinc phthalocyanine (ZnPC)-encapsulating liposomes. Following a 30-minute incubation with liposomes, the cells were either left untreated or treated at low (50 mW) or high (500 mW) laser power (cumulative light dose of 15 J/cm2). Cells were harvested 90 minutes post-PDT and whole genome expression analysis was performed using Illumina HumanHT-12 v4 expression beadchips. Hilar cholangiocarcinoma (SK-ChA-1) cells were incubated with PBS (control group) or 500 Î¼M zinc phthalocyanine (ZnPC)-encapsulating liposomes (ZnPC-ITLs, final lipid concentration). After 30 minutes, cells that were incubated with ZnPC-ITLs were either kept in the dark (ITL group) or were treated with 500-mW (ITL 500) or 50-mW (ITL 50) laser light (n = 3 per group, cumulative light dose of 15 J/cm2). Ninety minutes after photodynamic therapy, total cellular RNA was isolated and gene expression levels were analyzed by using the Illumina HumanHT-12 v4 platform. The data was analyzed in the context of survival signalling and comparisons were made with the control group.

Dataset Information

Phosphoproteomics of PDT treated SK-ChA-1 cells

Publications

Multi-OMIC profiling of survival and metabolic signaling networks in cells subjected to photodynamic therapy.

Similar Datasets

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