TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma
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PROVIDER: PRJNA157301 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. Thus we explored the target microRNA of TLS-CHOP influence cell-proliferation or cell death with microarray. MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. In this study, we have found that miR-486-5p (miR-486) expression level was downregulated by ectopic expression of TLS-CHOP fusion gene in mouse fibroblast cells (NIH3T3). In addition, we found overexpression of miR-486 inhibited the cell growth in the 2645/94 cells and in situ hybridization of miR-486 showed MLS tissues had lower signal intensity compared with non-tumor tissues. Thus we explored the target genes of miR-486 influence cell-proliferation or cell death with microarray. We compared the microRNA profiles of cells treated with TLS-CHOP or empty vector about NIH-3T3 cell-line. We compared the whole mRNA profiles of cells transfected with miR-486 oligonucleotides or control oligo about myxoid liposarcoma cell-line.
2013-03-23 | E-GEOD-36966 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. Thus we explored the target microRNA of TLS-CHOP influence cell-proliferation or cell death with microarray. MicroRNAs (miRNAs, miRs) are small noncoding RNAs, which control or are controlled by the dysregulation of multiple protein-coding oncogenes or tumor suppressor genes, play important roles in carcinogenesis. Myxoid liposarcomas (MLS) are characterized by t(12;16)(q13;p11) translocation and expression of TLS/CHOP chimeric transcripts (various types) which encode different oncogenic proteins. TLS-CHOP is important for the molecular mechanisms in the development of MLS, but the involvement in microRNA expression still remain poorly understood. In this study, we have found that miR-486-5p (miR-486) expression level was downregulated by ectopic expression of TLS-CHOP fusion gene in mouse fibroblast cells (NIH3T3). In addition, we found overexpression of miR-486 inhibited the cell growth in the 2645/94 cells and in situ hybridization of miR-486 showed MLS tissues had lower signal intensity compared with non-tumor tissues. Thus we explored the target genes of miR-486 influence cell-proliferation or cell death with microarray.
2013-03-23 | GSE36966 | GEO
Project description:The TLS-CHOP fusion protein is found in the majority of human myxoid liposarcomas (MLS), and is thought to have oncogenic functions. Until now, however, the molecular function of TLS-CHOP for oncogenesis is still elusive. In this report, we have revealed that knockdown of TLS-CHOP by specific siRNA in MLS-derived cell lines inhibits cell growth and leads to cell death. Thus, TLS-CHOP may be a promising therapeutic target for MLS treatment. Thus we explored the target genes of TLS-CHOP influence cell-proliferation or cell death with microarray. We compared the whole mRNA profiles of cells treated with TLS-CHOP siRNA or control oligo in two myxoid liposarcoma cell-line.
2013-12-27 | E-GEOD-33616 | biostudies-arrayexpress
Project description:The TLS-CHOP fusion protein is found in the majority of human myxoid liposarcomas (MLS), and is thought to have oncogenic functions. Until now, however, the molecular function of TLS-CHOP for oncogenesis is still elusive. In this report, we have revealed that knockdown of TLS-CHOP by specific siRNA in MLS-derived cell lines inhibits cell growth and leads to cell death. Thus, TLS-CHOP may be a promising therapeutic target for MLS treatment. Thus we explored the target genes of TLS-CHOP influence cell-proliferation or cell death with microarray.
2013-12-27 | GSE33616 | GEO
Project description:We identified novel protein-protein interactions between FUS-CHOP, a fusion oncoprotein that drives myxoid liposarcoma, and SNF2H, the ATPase subunit of the imitation switch (ISWI) chromatin remodeling complex. We used antibodies for FUS-CHOP, SNF2H, and H3K27ac to profile localization of these proteins and histones marks on chromatin in human MLPS cell lines and show that colocalization of FUS-CHOP and SNF2H occurs at new enhancers marked by H3K27ac.
2022-02-21 | GSE145678 | GEO
Project description:FUS-CHOP and ISWI chromatin remodeling in human myxoid liposarcoma
| PRJNA607943 | ENA
Project description:Myxoid liposarcoma (LS), the most common subtype of LS, is known to be characterized by the specific t(12;16) resulting in a TLS-CHOP fusion in almost all cases. We wished to address the following questions: (i) Is this genetic hallmark also present in other types of LS with predominant myxoid change? (ii) What is the proportion of cases with the variant EWS-CHOP fusion? (iii) What is the optimal approach for Southern blot detection of TLS breakpoints? We identified 59 LS characterized histologically by >90% myxoid component, in which frozen tissue tumor was available for DNA extraction. These 59 LS with myxoid features were divided into 2 groups: 42 LS with classic myxoid/round cell appearance (myxoid LS) and 17 well-differentiated LS (WDLS) with a predominant (>90%) myxoid component. Within the myxoid LS group, 29 tumors were low grade and 13 high grade (>20% round cell component). Among the 17 predominantly myxoid WDLS, there were 15 low grade and 2 focally high grade tumors. In addition, we selected as control group, 20 LS of other histological types with minimal or no myxoid change (17 WDLS and 3 pleomorphic LS) and 13 myxofibrosarcomas. Southern blot analysis was performed in all cases using a CHOP cDNA probe, and in all CHOP rearranged cases using a TLS cDNA probe. Probe/enzyme combinations for Southern blot analysis were CHOP exon 3-4 cDNA probe with BamHI or SacI, TLS exon 3-6 cDNA probe with BclI. All 42 cases of myxoid LS showed a CHOP rearrangement and 38 of them also had a TLS rearrangement. Among the 4 myxoid LS without Southern blot evidence of TLS rearrangement, 1 showed an EWS-CHOP fusion by Southern blotting and reverse transcriptase-polymerase chain reaction and in another case, reverse transcriptase-polymerase chain reaction detected a TLS-CHOP fusion transcript. None of the predominantly myxoid WDLS and none of the tumors included in the control group showed rearranegements with CHOP probe. In addition, 12 predominantly myxoid WDLS, 10 other LS, and 5 myxofibrosarcoma from the control group were also tested for TLS rearrangement; all were negative. The TLS-CHOP fusion is highly sensitive and specific for the entity of classic myxoid/round cell LS. Other types of LS, even with a predominant myxoid component, lack the TLS-CHOP rearrangement, confirming that they represent a genetically distinct group of LS. The prevalence of the EWS-CHOP variant fusion was approximately 2% in this series. The optimal enzyme for TLS genomic breakpoint detection is BclI.
| S-EPMC1906905 | biostudies-literature
Project description:Transcriptional profiling of patient-derived xenograft models of myxoid liposarcoma with either FUS-CHOP type I, named as ML017, or FUS-CHOP type III, named as ML006. Both ML017 and ML006 are responsive to trabectedin treatment, while model ML017/ET has aquired resistance to the drug. Samples are either under untreated conditions, or treated either with trabectedin or pioglitazone or both.
2020-01-10 | E-MTAB-8632 | biostudies-arrayexpress
Project description:In order to identify new key molecules in the pathogenesis of myxoid liposarcoma, we performed comparative gene expression profiling in myxoid liposarcoma and fat tissue samples.
2014-10-28 | GSE62747 | GEO
Project description:In order to identify new key molecules in the pathogenesis of myxoid liposarcoma, we performed comparative gene expression profiling in myxoid liposarcoma and fat tissue samples. Whole genome microarray analysis was performed on eight primary myxoid liposarcoma samples and an RNA pool of eight healthy fat tissue samples.
2014-10-28 | E-GEOD-62747 | biostudies-arrayexpress