Resitant populations to photodynamic therapy (PDT) of squamous cell carcinoma cells (SCC-13)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE180325 | GEO | 2021/07/21
REPOSITORIES: GEO
Similar Datasets
Project description:aCGH of control cells not subjected to PDT (Parental) and cells subjected to 5 or 10 sequential PDT treatments (5ºG and 10ºG, respectively).
2013-09-06 | GSE50602 | GEO
Project description:aCGH of control cells not subjected to PDT (Parental) and cells subjected to 5 or 10 sequential PDT treatments (5M-BM-:G and 10M-BM-:G, respectively). Three-condition experiment, cultures of SCC-13 cells not subjected to PDT (Parental) vs 5M-BM-:G and 10M-BM-:G generations of resistant cells.
2013-09-06 | E-GEOD-50602 | biostudies-arrayexpress
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-κB)-, hypoxia-inducible factor 1-alpha (HIF-1α)-, 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.
2016-01-04 | GSE68292 | GEO
Project description:Resitant populations to photodynamic therapy (PDT) of squamous cell carcinoma cells (SCC-13)
| PRJNA747827 | ENA
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-κB)-, hypoxia-inducible factor 1-alpha (HIF-1α)-, 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 μM 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.
2016-01-04 | E-GEOD-68292 | biostudies-arrayexpress
Project description:Photodynamic therapy (PDT) is a tumor treatment strategy that relies on the production of reactive oxygen species (ROS) in the tumor following local illumination. Although PDT has shown promising results in the treatment of non-resectable perihilar cholangiocarcinoma, it is still employed palliatively. In this study, tumor-comprising cells (i.e., cancer cells, endothelial cells, macrophages) were treated with the photosensitizer zinc phthalocyanine that was encapsulated in cationic liposomes (ZPCLs). Post-PDT survival pathways were studied following sublethal (50% lethal concentration (LC50)) and supralethal (LC90) PDT using a multi-omics approach. ZPCLs did not exhibit toxicity in any of the cells as assessed by toxicogenomics. Sublethal PDT induced survival signaling in perihilar cholangiocarcinoma (SK-ChA-1) cells via mainly hypoxia-inducible factor 1 (HIF-1)-, nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-кB)-, activator protein 1 (AP-1)-, and heat shock factor (HSF)-mediated pathways. In contrast, supralethal PDT damage was associated with a dampened survival response. (Phospho)proteomic and metabolomic analysis showed that PDT-subjected SK-ChA-1 cells downregulated proteins associated with epidermal growth factor receptor (EGFR) signaling, particularly at LC50. PDT also affected various components of glycolysis and the tricarboxylic acid cycle as well as metabolites involved in redox signaling. In conclusion, sublethal PDT activates multiple pathways in tumor parenchymal and non-parenchymal cells that, in tumor cells, transcriptionally regulate cell survival, proliferation, energy metabolism, detoxification, inflammation/angiogenesis, and metastasis. Accordingly, sublethally afflicted tumor cells are a major therapeutic culprit. Our multi-omics analysis unveiled multiple druggable targets for pharmacological intervention.
2016-11-25 | GSE84757 | GEO
Project description:Photodynamic therapy (PDT) is a tumor treatment strategy that relies on the production of reactive oxygen species (ROS) in the tumor following local illumination. Although PDT has shown promising results in the treatment of non-resectable perihilar cholangiocarcinoma, it is still employed palliatively. In this study, tumor-comprising cells (i.e., cancer cells, endothelial cells, macrophages) were treated with the photosensitizer zinc phthalocyanine that was encapsulated in cationic liposomes (ZPCLs). Post-PDT survival pathways were studied following sublethal (50% lethal concentration (LC50)) and supralethal (LC90) PDT using a multi-omics approach. ZPCLs did not exhibit toxicity in any of the cells as assessed by toxicogenomics. Sublethal PDT induced survival signaling in perihilar cholangiocarcinoma (SK-ChA-1) cells via mainly hypoxia-inducible factor 1 (HIF-1)-, nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-кB)-, activator protein 1 (AP-1)-, and heat shock factor (HSF)-mediated pathways. In contrast, supralethal PDT damage was associated with a dampened survival response. (Phospho)proteomic and metabolomic analysis showed that PDT-subjected SK-ChA-1 cells downregulated proteins associated with epidermal growth factor receptor (EGFR) signaling, particularly at LC50. PDT also affected various components of glycolysis and the tricarboxylic acid cycle as well as metabolites involved in redox signaling. In conclusion, sublethal PDT activates multiple pathways in tumor parenchymal and non-parenchymal cells that, in tumor cells, transcriptionally regulate cell survival, proliferation, energy metabolism, detoxification, inflammation/angiogenesis, and metastasis. Accordingly, sublethally afflicted tumor cells are a major therapeutic culprit. Our multi-omics analysis unveiled multiple druggable targets for pharmacological intervention.
2016-11-25 | GSE84756 | GEO
Project description:This proteomic study This proteomic study focuses on the role of reversible thiol oxidation after hexyl aminolevulinate mediated PDT (HAL-PDT). The human epidermoid carcinoma cell line A431 was used as model system and red light as light source, a clinical relevant in vitro model. The light dose dependent cell cytotoxicity was measured by resazurin assay. The most clinical relevant dose, LD100, was used for the proteomic part of the study and cells where harvested 30 min after treatment. The reversibly oxidized thiol proteins were selected by biotinylation and identified by mass spectrometry. This proteomic technique revealed over 1100 thiol proteins which were reversibly oxidized after HAL-PDT. Identified proteins were analysed by bioinformatics (IPA and GO) and a list of reliable identified proteins (282 proteins) where further analysed. Both the cellular location and function was determined for these proteins. In addition, 18 of the proteins where identified as redox regulated, 36 to be a part of the apoptotic pathway and 9 to be both redox regulated and a part of apoptotic pathway. From these results we suggest redox regulated proteins as a trigger mechanism for PDT induced apoptosis.focuses on the role of reversible thiol oxidation after hexyl aminolevulinate mediated PDT (HAL-PDT). The human epidermoid carcinoma cell line A431 was used as model system and red light as light source, a clinical relevant in vitro model. The light dose dependent cell cytotoxicity was measured by resazurin assay. The most clinical relevant dose, LD100, was used for the proteomic part of the study and cells where harvested 30 min after treatment. The reversibly oxidized thiol proteins were selected by biotinylation and identified by mass spectrometry. This proteomic technique revealed over 1100 thiol proteins which were reversibly oxidized after HAL-PDT. Identified proteins were analysed by bioinformatics (IPA and GO) and a list of reliable identified proteins (282 proteins) where further analysed. Both the cellular location and function was determined for these proteins. In addition, 18 of the proteins where identified as redox regulated, 36 to be a part of the apoptotic pathway and 9 to be both redox regulated and a part of apoptotic pathway. From these results we suggest redox regulated proteins as a trigger mechanism for PDT induced apoptosis.
2016-01-12 | PXD001582 | Pride
Project description:Cancer is a global leading cause of death, with nearly 10 million people dying from cancer in 2020. Photodynamic therapy (PDT) has emerged as a promising cancer treatment modality; however, the potential molecular mechanisms remain obscure. Herein, we designed a near-infrared (NIR) light-activated nanoplatform (TPBC-PEG) to explore the therapeutic effects and mechanisms of PDT by using a model of intratibial primary and pulmonary metastasis osteosarcoma. Under laser irradiation, TPBC-PEG photosensitizer dose-dependently inhibited proliferative and metastatic capability while promoting apoptosis of osteosarcoma cells in vitro, and also effectively suppressed carcinogenesis and pulmonary metastasis in osteosarcoma xenograft mouse model. Moreover, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis after high-throughput mRNA-seq indicated that the HIPPO signaling pathway was one of the 20 most significantly related signaling pathways. And a series of experiments for determining the HIPPO signaling activity were conducted to reconfirm the specificity. Collectively, PDT of TPBC-PEG micelles against carcinogenesis and pulmonary metastasis of deep-seated intratibial osteosarcoma was achieved by activating HIPPO signaling pathway. Our study identified a hitherto uncharacterized molecular mechanism of PDT, which may provide new insights to understand and design promising nanoplatforms for future cancer therapies.
2023-08-25 | GSE211393 | GEO
Project description:We report the application of 5-ALA ( 5-Aminolevulinic acid)-mediated photodynamic therapy on mouse brain tissue, and further explored the impact of PDT on nervous system.
2021-04-30 | GSE173615 | GEO