Project description:We performed RNA sequencing to assess changes in gene expression in lung cancer cell lines. Total RNA was extracted from the cells, before and after stimulation with IFNγ, using standard approaches. RNA-sequencing data performed in this work was performed and analyzed at the CNAG-CRG.
Project description:RNA sequencing was performed on HCT116 and HKE3 colorectal cancer cell lines before stimulation and at 15, 30, 60, 90 and 120 mins post-stimulation with transforming growth factor alpha (TGF-α) (0.01 µg/mL, Abcam). Three replicates were sequenced at each time point.
Project description:Identification and comparison of genes induced by IRF1 ectopic expression versus IFNγ treatment in A549 lung epithelial fibroblasts.
Project description:Infections can trigger the release of IFNγ, a type II interferon, which exacerbates tissue inflammation and may lead to severe acute lung injury (ALI). However, the regulatory mechanisms of IFNγ production in the lungs are not fully understood. In this study, we identified RGS2 as a crucial regulator of IFNγ levels in the lungs during infection. The absence of RGS2 led to persistently elevated IFNγ production in macrophages, resulting in unresolved inflammatory lung damage. Notably, this effect was absent in RGS2-deficient chimeric mice that received wild-type bone marrow or RGS2 expression in alveolar macrophages (AMs), as well as in those treated with an IFNγ-blocking antibody. RGS2 exerts its regulatory role by inhibiting Gαq-mediated IFNγ production and inflammatory signaling in AMs. Consequently, the inhibition of Gαq in RGS2-deficient mice prevented IFNγ production in AMs and shifted their transcriptomic profile from an inflammatory to a reparative state. These findings suggest that the RGS2-Gαq signaling pathway could be a promising therapeutic target for mitigating inflammatory lung injury.
Project description:RNA sequencing was performed on wtHKE3 and mtHKE3 colorectal cancer cell lines (obtained from Shirasawa [1]) before stimulation (timepoint 0) and at 15, 30, 60, 90 and 120 mins post-stimulation with transforming growth factor alpha (TGF-α) (0.01 µg/mL, Abcam). Three replicates were sequenced at each timepoint. [1] Tsunoda, Ishikura, Doi et al., Anticancer Res 2015, 35(8):4453-4459.
Project description:PRC2-isogenic human malignant peripheral nerve sheath tumor (MPNST) M3 cells were generated through CRISPR/Cas9-mediated knockout of the PRC2 core component, SUZ12. PRC2 loss led to not only significant increase, but also significant decrease of chromatin accessibility at 15,346 (16% of all ATAC peaks) and 20,099 genomic loci (21% of all ATAC peaks), respectively. PRC2 loss decreased the chromatin accessibility for IFNγ-responsive loci in M3 cells, resulting in dampened response to IFNγ stimulation.