Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. The aim of this experiment is to study the impact of gal-9 gene invalidation in the colon carcinoma cell line CT26, in vitro. It complements the results of a RNAseq analysis carried out using the same cells, whose results are already available on Annotare (E-MTAB-9559)
Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. The aim of this experiment is to study the impact of gal-9 gene invalidation in the colon carcinoma cell line CT26, in vitro.
Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. The aim of this experiment is to study the impact of gal-9 gene invalidation in the murine bladder carcinoma cell line MB49, in vitro. It complements the results of : 1) a RNAseq analysis performed on in vitro cell cultures ; 2) a comparative experiment carried out using the same cells as part of a serial transplantations protocol, whose results are already available on Annotare (E-MTAB-9570 ; E-MTAB-9220).
Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. The aim of this experiment is to study the impact of gal-9 gene invalidation in the murine bladder carcinoma cell line MB49, in vitro. It complements the results of a comparative experiment carried out using the same cells as part of a serial transplantations protocol, whose results are already available on Annotare (E-MTAB-9220).
Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. So far, all animal studies on this subject have been focused on gal-9 released by infiltrating cells, without paying attention to gal-9 released by malignant cells. To address this issue, we derived by gene editing, isogenic clones - either positive or negative for gal-9 - from the MB49 murine bladder carcinoma cell line. A progressive reduction of tumor growth was observed when gal-9-KO cells were subjected to serial transplantations into syngenic mice but not into nude mice thus accounting the tumor growth reduction in syngenic mice to a better immune response. Tumor fragments were collected from WT and KO tumors at different steps of the experiment : 2nd growth cycle (WT = 5 samples ; KO = 6 samples ) ; 3rd growth cycle (WT = 5 samples ; KO = 7 samples) ; 4th growth cycle (WT = 4 samples ; KO = 3 samples), in order to study the differences between WT and KO tumors through the serial transplantations, by RNAseq analysis.
Project description:USP8 is one of DUBs and is frequently overexpressed or gain-of-function mutated in multiple types of human cancer. Importantly, USP8 has been identified as an immunomodulatory DUB as T cell-specific Usp8 deficiency disrupts regulatory T cell functions, leading to recruiting abundant CD8+ T cells in colons and resulting in the inflammatory bowel disease in mice. However, whether targeting USP8 can enhance anti-tumor immunity has not been reported. To further explore the physiological function of USP8, we performed the transcriptomic analysis to comprehensively understand which signaling pathways are mainly regulated by USP8 in cancer cells. Usp8 WT and KO CT26 cells were harvested for RNA-sequencing (RNA-seq).