Project description:STAT2 is an essential transcription factor in type I interferon (IFN) signaling. STAT2 mediates the antigrowth and apoptotic effects of IFN as demonstrated in cell lines thus leading to the hypothesis that STAT2 has tumor suppressor function. We used microarrays to identify genes in the tumors that are STAT2 dependent and important in anti-tumor immunity. B16-F1 melanoma tumor cells were implanted on the dorsal flank of either wild type (WT) or Stat2KO (S2KO). Tumor growth was monitored during the course of 3 weeks. S2KO mice developed larger tumors when compared to WT mice.
Project description:B cells potentially play a role in the immune response to melanoma, including during treatment with immune modulators. We profiled (transcriptome analysis) effects of anti-PD-L1 antibody therapy on gene expression in B16 melanoma tumors of B cells depleted and WT syngeneic mice. After 7 days of B16 tumors implantation, mice were treated or untreated with anti-PD-L1 antibody (every three days).
Project description:To investigate the impact of Card11 on TIL differentiation, we isolated TILs from B16-F10 tumors of WT mice, E134G mice, and K215M mice and performed scRNA seq. We also sorted tumor-infiltrating lymphocytes (TILs) from melanoma(B16-F10) of WT mice and conducted scRNA and scTCR sequencing. To further investigate the impact of Card11 on TCR clonal diversity, we sorted CD8 T cells from melanoma WT mice or K215M mice and performed scRNA and scTCR sequencing.
Project description:B16 melanoma cells were screened with a CRISPR library against TSGs in vitro and as tumors in Rag1-null and immunocompetent WT C57BL/6 mice
Project description:To identify the co-immunoprecipitating proteins of Rab27a following Rab27a pull down of B16-F1 mouse melanoma cells infected with adenovirus expressing GFP-hsSPIRE1.
Project description:The goal of this study was to compare the gene expression profiles of a highly versus poorly tumorigenic murine melanoma. B16-F1 is a well-characterized murine melanoma cell line that grows progressively in hosts, both as primary tumors in subcutaneous tissue and as metastatic lesions in internal organs. D5.1G4 is a chemically mutated variant of B16 melanoma that grows with significantly slower kinetics than its wild-type counterpart. Whole genome expression microarray analysis of RNA isolated from these murine melanoma lines was performed to provide insights into factors that regulate the growth and metastasis of these tumors, which are useful models for investigating in a murine system the outgrowth, progression, and control of a cancer type that is prevalent in humans worldwide.
Project description:The FOXC2 transcription factor regulates a variety of developmental and biological processes in both embryonic and adult tissues. Importantly, overexpression or dysregulation of FOXC2 is also associated with oncogenic activity in numerous cancer types, though the function of FOXC2 in the context of melanoma has not been previously investigated. Therefore, the goal of this study was to assess FOXC2's regulation of gene expression in melanoma cells. To this end, we employed CRISPR-Cas9 gene editing technology to disrupt the Foxc2 gene in B16-F1 melanoma, and we performed RNA-seq analysis to assess differential gene expression between the wild-type B16-F1 melanoma cell line and our novel FOXC2-deficient B16-F1ΔFOXC2 gene-edited variant cell line.
Project description:B cells potentially play a role in the immune response to melanoma, including during treatment with immune modulators. We profiled effects of 3M-052 on gene expression in draining lymph nodes of syngeneic mice bearing B16 melanoma tumors. When B16 tumors reached 30-40 mm2 in size, they were injected intratumorally once with 3M-052 or vehicle control.
