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Genes up-regulated in T24 (bladder cancer) cells in response to the photodynamic therapy (PDT) stress.

PAG Title Genes up-regulated in T24 (bladder cancer) cells in response to the photodynamic therapy (PDT) stress.
PAG ID MAX000336
Type A
Source Link MSigDB
Publication Reference NA
PAG Description Photodynamic therapy (PDT) is an anticancer approach utilizing a light-absorbing molecule and visible light irradiation to generate, in the presence of O(2), cytotoxic reactive oxygen species, which cause tumor ablation. Given that the photosensitizer hypericin is under consideration for PDT treatment of bladder cancer we used oligonucleotide microarrays in the T24 bladder cancer cell line to identify differentially expressed genes with therapeutic potential. This study reveals that the expression of several genes involved in various metabolic processes, stress-induced cell death, autophagy, proliferation, inflammation and carcinogenesis is strongly affected by PDT and pinpoints the coordinated induction of a cluster of genes involved in the unfolded protein response pathway after endoplasmic reticulum stress and in antioxidant response. Analysis of PDT-treated cells after p38(MAPK) inhibition or silencing unraveled that the induction of an important subset of differentially expressed genes regulating growth and invasion, as well as adaptive mechanisms against oxidative stress, is governed by this stress-activated kinase. Moreover, p38(MAPK) inhibition blocked autonomous regrowth and migration of cancer cells escaping PDT-induced cell death. This analysis identifies new molecular effectors of the cancer cell response to PDT opening attractive avenues to improve the therapeutic efficacy of hypericin-based PDT of bladder cancer.
Species Homo sapiens
Quality Metric Scores nCoCo Score: 46
Information Content Rich
Other IDs M6782
Base PAG ID MAX000336
Human Phenotyte Annotation
Curator PAGER curation team
Curator Contact PAGER-contact@googlegroups.com
Gene ID Gene symbol Gene name RP_score
Gene A Gene B Source SCORE

Gene A Gene B Mechanism Source
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