Project description:The efficacy of photodynamic therapy for treating premalignant and malignant tumors is often limited by the emerging resistant tumor cells. We have developed experimental model systems to study the mechanisms associated with resistance to photodynamic therapy induced by structurally similar photosensitizers (two novel porphyrin-based photosensitizers and temoporfin) in mouse mammary carcinoma cell line 4T1. Photodynamic therapy resistant clones were obtained in vitro by exposure to constant photosensitizer concentration and irradiation with increasing light doses.
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.
Project description:The goal of the study was to determine whether photodynamic oncolytic virus therapy of glioblastoma and malignant meningioma xenografts in mice alters transciptomics associated with efficacy. RNA sequencing was used from tumors treated with PBS, laser, G47delta-KillerRed, and G47delta-KillerRed and laser, which is photodynamic oncolytic virus therapy.
Project description:Study of the gene expression of T24 bladder cancer cells in response to hypericin-mediated photodynamic therapy in the absence or presence of the p38 MAPK inhibitor PD169316
Project description:Human tumour cell lines PC3, DU145, U87 and U373 (prostate carcinoma and glioblastoma) were treated with photosensitizers 5-aminolaevulinic acid (5-ALA) or photofrin. Then, the cells were irradiated sublethally with 635 nm laser light.<br>After photodynamic therapy, the cells were grown at 37°C for 4 or 24 hours in the dark until extraction of total RNA and expression profiling.
Project description:We report the application of Porfimer sodium-mediated photodynamic therapy on mouse brain endothelial cells, and further identified the impact of PDT on the normal vessel cells.
Project description:We used selenium as a photodynamic anti-tumor synergist of phycocyanin to explore its inhibitory effect on lung cancer and its molecular mechanism in vitro. First of all, we used LLC-luc mouse lung cancer cells to establish a tumor-bearing model. Selenium-enriched phycocyanin was injected next to the tumor. When it was absorbed by the tumor tissue, the tumor site was irradiated by a 620nm wavelength laser. The changes in tumor size were monitored in real-time and the physiological indexes of mice were measured. It was found that selenium phycocyanin photodynamic therapy could enhance the inhibitory effect of tumors and improve the level of antioxidation in tumor-bearing mice. In addition, the pathological section observation and electron microscope microstructure analysis of the tumor tissue showed that the effect of the selenium-enriched phycocyanin photodynamic treatment group was more significant. At the same time, the tumor tissue transcriptional group sequencing analysis and qRT-PCR verification analysis showed that selenium-enriched phycocyanin photodynamic treatment group could reduce the expression of Mmp13, Serpine1, Vegfa, and Ppbp genes inhibit tumor cell metastasis and proliferation, up-regulate the expression of Ccl2, Ccl3, Cxcl2 and down-regulate the expression of Ccl24 chemokine, and promote tumor local immunity. Our results show that selenium phycocyanin photodynamic therapy plays an anti-tumor effect by promoting tumor cell apoptosis, reducing inflammation, and promoting tumor immunity.
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.
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.
