Project description:extracellular PTEN treatment did not affect the growth of PTEN knockout B16-F10 cells cultured in vitro. , To investigate whether extracellular PTEN act on the tumor microenvironment to exert a tumor-suppressive role in vivo，molecular changes caused by PTEN treatment inside the B16-F10-PTEN tumors were monitored by RNA sequencing.
Project description:To analyze the effects of Cdh1 signaling on melanoma properties, we performed microarray analysis to identify genes induced by soluble Cdh1 in mouse melanoma cell line B16-F10.
Project description:IRF4 deficient NK cells displayed more resistant to exhaustion during B16-F10 metastasis, to investigate how IRF4 deletion enhances the resistance of NK cells to exhaustion, we sorted NK cells from WT and Irf4-/- mice ingected with B16-F10 or not for RNA-seq
Project description:The mouse melanoma cell line B16-F10 provided by American Type Culture Collection (ATCC® CRL-6475™) were treated with DMSO, G007-LK, WNT or G007-LK+WNT, done in triplicates for a total of 12 samples.
Project description:PTEN treatment can affect the tumor growth of PTEN knockout B16-F10 cells in C57BL/6J mice，We hope to analyze the changes that occur in various cells in tumors through single-cell RNA sequencing.
Project description:We previously showed that transgenic enhancement of histamine production in B16-F10 melanomas strongly supports tumor growth in C57Bl/6 mice (Cancer Res, 2005 Pos et al.). In this array experiment, gene expression profiles of transgenic mouse melanomas, secreting different amounts of histamine, were compared by whole genome microarrays. Experiment Overall Design: By modifying the levels of L-histidine decarboxylase (HDC), the sole enzyme responsible for histamine production, we introduced three novel variants of the B16-F10 mouse melanoma cell line, displaying diminished (B16-F10 HDC-A), unmodified (B16-F10 HDC-M) or enhanced (B16-F10 HDC-S) capacities to produce and secrete histamine. Experiment Overall Design: In this experiment, B16-F10 HDC-A, HDC-M, and HDC-S experimental mouse melanomas were compared by analyzing 6-6 tumors in each group. Experiment Overall Design: In order to reduce the amount of arrays required, equal amounts of randomly chosen RNA sample pairs were pooled in each group, thus, at the end, each group consisted of 3 pooled tumor samples. All samples were biological replicates, no technical replicates or dye swapping were done. Experiment Overall Design: Gene expression patterns of the three tumor groups were compared indirectly, via a common reference samplei n a two-color array design. Arrays shown here represent gene expression patterns of individual tumor samples compared to the reference sample.
Project description:Proteome analysis of Lung tissue of mice bearing B16-F10-luc-G5 melanoma tumor with sleep fragmentation and with or with out the asdmistration of GL-pp. The mice were randomly divided into 4 groups: control group in general condition with no further treatment (CON group), tumor group with the burden of B16-F10-luc-G5 cells (Tumor group), T+SF group with SF and the burden of B16-F10-luc-G5 cells (T+SF group), and GL-pp group with SF, tumor cells burden, and the administration of 80 mg/kg GL-pp (GL-pp group). B16-F10-luc-G5 cells (5 × 1000000 cells/100 µL per mouse) were injected into the mice through the tail vein. The lung tissue of T+SF group and GL-pp group were analyzed by the proteome.
Project description:B16 F10 is a depigmented mouse melanoma cell line which is considered as a homogeneous cell population. These cells when cultured at a very low density of 100 cells/cm2 starts to pigment progressively. We used single nucleus RNA+ATAC sequencing (scMultiomics) to analyze the transciptional diversity and to investigate the epigenetic basis of this diversity of day 0, 3 and 5 B16 cells cultured at low density.
Project description:To investigate the cooperative function LUBAC E3 ligase complex during tumor development, we established HOIP-knockout B16-F10 murine melanoma cell lines.
