Chip-chip from HCT116 cells with YBX1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18337 | GEO | 2010/10/09
SECONDARY ACCESSION(S): PRJNA118003
REPOSITORIES: GEO
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Project description:YBX1 is a multifunctional protein involved in the control of transcription and translation. We identified YBX1 as an target of MEK/ERK signaling in colorectal cancer cell lines. We performed a ChIP-chip analysis of HCT116 cells to identify new potential target genes of YBX1. Comparison of input DNA fragments with fragments coprecipitated with YBX1 in HCT116 cells.
2010-10-09 | E-GEOD-18337 | biostudies-arrayexpress
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Project description:In order to identify YBX1-dependent targets that are modulated under hypoxic conditions, we used control and YBX1 knockdown cells grown under normoxia and hypoxia to profile gene expression levels. Control and YBX1-knockdown cells were grown and profiled under hypoxia and normoxia to identify YBX1-dependent hypoxia-induced target transcripts.
2015-05-08 | E-GEOD-63562 | biostudies-arrayexpress
Project description:In order to identify YBX1 binding sites on endogenous RNA, we performed HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Licatalosi D, et al. 2008, Nature 456:464-U22)
2015-05-08 | E-GEOD-63604 | biostudies-arrayexpress
Project description:Breast cancer is the second leading cause of death in women worldwide, with triple-negative breast cancer (TNBC) having the worst prognosis. Although there are numerous studies on TNBC, there is no effective treatment for it, and it is still a major problem today. Studies on PIWI-interacting RNAs (piRNAs) are increasing and investigating the mechanism of piRNAs in the proliferation and metastasis of TNBC may lead to new potential treatment targets. Here, we identified a novel piRNA, piR-YBX1, which was downregulated in TNBC compared to matched normal breast tissue. Overexpression of piR-YBX1 significantly inhibited the proliferation, migration, invasion ability of TNBC cells both in vivo and in vitro. Mechanistically, piR-YBX1 could bind directly to mRNA of YBX1 and overexpression of piR-YBX1 downregulated YBX1 in both mRNA and protein levels, while the function of piR-YBX1 could be partly rescued by overexpression of YBX1. In addition, YBX1 could bind to RAF1 which is the key molecule in the MAPK signaling pathway, and overexpression of piR-YBX1 inhibited the p-MEK and p-ERK1/2 which can be reverted by YBX1. In conclusion, our findings discovered that the piR-YBX1/YBX1/MAPK axis suppresses the proliferation and metastasis of TNBC and therefore piR-YBX1 has the potential to be an effective therapeutic agent for breast cancer.
2023-11-01 | GSE245714 | GEO
Project description:In order to identify YBX1 binding sites on tRNA fragments, we performed small-RNA HITS-CLIP on endogenous YBX1 We used a previously published method to perform HITS-CLIP on endogenous YBX1 (Chi SW, et al. 2009, Nature 460:479)
2015-05-08 | E-GEOD-63597 | biostudies-arrayexpress
Project description:In order to test whether inhibition of tRFs induced under hypoxia would counteract the YBX1-dependent reduction of target transcripts, we used transient transfection of antisense locked-nucleic acids (pooled LNAs) against tRFAsp, tRFGly, tRFGlu, and tRFTyr under hypoxia followed by microarray profiling. Synthetic antisense locked-nucleic acids (LNAs) targeting the YBX1 binding site on tRFAsp, tRFGly, tRFGlu, and tRFTyr were transfected (as a pool) in control and YBX1-knockdown cells under hypoxia to assess the consequences of inhibiting tRFs induced in hypoxic MDA-parental cells.
2015-05-08 | E-GEOD-63563 | biostudies-arrayexpress
Project description:The chromatin remodeller p400 has oncogenic properties that promote early steps of colon cancer. Chromatin immunoprecipitation (ChIP) of p400 together with chromatin profiling by ChIP-on-chip analysis demonstrated that p400 directly binds the chromatin at promoters of p400 target genes. Study of p400 binding on promoters of HCT116 cells
2013-11-22 | E-GEOD-45614 | biostudies-arrayexpress
Project description:Janus kinases (Jak) mediate cytokine, hormone and growth factor responses in hematopoietic cells. Jak2 is one of the most frequently mutated genes in the aging hematopoietic system and in hematopoietic cancers. Mutations in Jak constitutively activate downstream signaling and are drivers of myeloproliferative neoplasms (MPN). In clinical use, Jak-inhibitors have incomplete effects on overall disease burden of Jak2 mutated clones, prompting us to investigate the mechanism underlying disease persistence. By in-depth phospho-proteome profiling we here identify proteins involved in mRNA processing as targets of mutant Jak2. Inactivation of the post-translationally modified Jak2-target Ybx1 sensitizes Jak-inhibitor persistent cells to apoptosis and results in RNA mis-splicing, retained intron enrichment and disruption of the transcriptional control of extracellular signal-regulated kinase (ERK) signaling. In combination with pharmacological Jak-inhibition it induces apoptosis in Jak2-dependent murine and primary human cells, leading to in vivo regression of the malignant clones and inducing remission. This identifies and validates a novel cell-intrinsic mechanism how differential protein phosphorylation results in splicing-dependent alterations of Jak2-ERK-signaling and the maintenance of Jak2V617F malignant clones. Therapeutic targeting of Ybx1 dependent ERK-signaling in combination with Jak2-inhibition may eradicate Jak2-mutated cells.
2020-08-20 | PXD006921 | Pride
Project description:The perturbation of the genetic program due to mutational activation of KRAS- or BRAF-mediated signal transduction is a prerequisite for the expression of neoplastic phenotypes; however, the mechanisms of cancer cell-specific transcriptional deregulation are poorly understood. We have analyzed the human colorectal cancer cell lines HCT116, HT29 and SW480 using an integrated approach combining transcriptional profiling, small molecule inhibitors targeting signaling pathway effectors, and computational prediction of regulatory elements in promoters of co-expressed genes with chromatin-based and cellular assays. We identified groups of coexpressed genes involved in similar biological processes, demonstrating a link between biological function and transcriptional organization. Among them we found groups of proliferation associated genes which responded to MEK/MAPK inhibition in all three cell lines. We predicted by computational analysis of the promoter regions of these genes, that NFY binding sites might be important regulatory elements for the MEK/MAPK-dependent transcriptional control. We validated this prediction in reporter gene assays by using a fragment of the CCNB1 promoter as a model. We discovered YBX1 to be associated with the endogenous CCNB1 promoter and the promoters of 62 additional genes within the proliferation associated gene groups by a ChIP-on-chip assay. Silencing of YBX1 expression by siRNA prevents CCNB1 expression and partially inhibits proliferation of HCT116 cells. In view of multiple known YBX1 functions in stress response, chromatin remodeling, transcriptional and translational regulation, our results indicate that this factor may also contribute to RAS-induced pleiotropic effects in cancer. The cells were treated with certain inhibitors for 48 hours. We used one sample per cell line treated with DMSO as a control, and one sample for each of the treatments.
2010-10-09 | E-GEOD-18232 | biostudies-arrayexpress