Project description:We showed that in response to chemotherapy, dying cancer cells can secrete spliceosomal components into the extracellular space. These therapy-induced secretomes enriched with spliceosomal components promote the chemoresistance of recipient tumor cells. We demonstrated that spliceosomal proteins SNU13 and SYNCRIP can relocalize from dying tumor cells to recipient tumor cells via extracellular vesicles. To investigate whether the increased abundance of splicing factors could be the reason for the acquisition of a more aggressive phenotype by tumor cells, we got SKOV3 cell lines stably overexpressing SYNCRIP or SNU13. These cell lines were more resistant to cisplatin compared to control cell line expressing empty vector. Next, to investigate how the therapy response is formed in tumor cells with and without overexpression of spliceosomal proteins SNU13 or SYNCRIP, we performed RNAseq analysis of these cells before and 24 hours after cisplatin treatment. Enrichement analyses showed that in response to cisplatin, genes associated with DNA repair and cell cycle regulation were upregulated in cancer cell lines overexpressing SYNCRIP or SNU13 compared with control cells. This study revealed previously unknown signaling molecules in the microenvironment of ovarian cancer that have potential clinical significance.
Project description:SPARC-deficient mice have been shown to exhibit impaired glucose tolerance and insulin secretion, but the underlying mechanism remains unknown. We used microarrays to detail the global programme of gene expression and identified distinct classes of up-regulated and down-regulated genes changed by overexpressing SPARC.
Project description:To identify potential targets of NR3C2 overexpression, RNA sequencing was performed to compare the transcriptomes of control and NR3C2-overexpressing (NR3C2-OE) HK2 cells.
Project description:In this assay, we aimed to investigate whether ZFP661 co-binds target regions with CTCF. To achieve this, we performed ChIP-reChIP-seq in ZFP661-3HA overexpressing (OE) mESCs, where the 1st ChIP utilized anti-HA antibody, and the 2nd ChIP involved the use of anti-IgG and anti-CTCF antibodies, respectively. Our results demonstrate that ZFP661 co-binds target regions with CTCF.
Project description:Proteomic characterization of extracellular vesicles derived from bladder cancer cells overexpressing GSTO1 and treated with cisplatin.
Project description:We assessed changes in chromatin accessibility in H3.3K27M DIPG cell lines on knockdown of metabolic enzymes including HK2, GDH and IDH1
Project description:HK2 is expressed in the hepatocellular carcinoma cell line Huh7 while GCK is expressed in the normal hepatocyte. In order to analyze the functional consequences of the expression of one or other of the hexokinases (HK2 or GCK) we have invalidated the expression of HK2 and induced the expression of GCK in Huh7 cells. We analyzed transcriptome of both cell line