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TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma

ABSTRACT: 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.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE36966 | GEO | 2013/03/23

SECONDARY ACCESSION(S): PRJNA157301

REPOSITORIES: GEO

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TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma

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

The Chimeric Oncoprotein TLS-CHOP Represses Expression of the Anticancer Cytokine MDA-7/IL-24 in Myxoid Liposarcoma Cells

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

The Chimeric Oncoprotein TLS-CHOP Represses Expression of the Anticancer Cytokine MDA-7/IL-24 in Myxoid Liposarcoma Cells

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TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma

Project description:TLS-CHOP Fusion Oncoprotein Regulates MicroRNA-486 in Human Myxoid Liposarcoma

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Gene expression profiling of myxoid liposarcomas (training set INT-A)

Project description:FUS-CHOP and EWS-CHOP balanced translocations characterize myxoid liposarcoma which encompasses myxoid (ML) and round cell (RC) variants initially believed to be distinct diseases. Currently, myxoid and RC liposarcoma are regarded to represent the well differentiated and the poorly differentiated ends, respectively, within spectrum of myxoid liposarcoma where the fusion proteins blocking lipogenic differentiation play a role in tumor initiation while molecular determinants associated to progression to RC remain poorly understood. Activation of AKT pathway sustained by PIK3CA and PTEN mutations and growth factor receptor signalling such as RET and IGF1R have been recently correlated with the increasing of aggressiveness and RC. Aim of the present study is to elucidate molecular events involved in driving round cell progression analyzing two small series of MLS selected to be representative of the two end of the gamut: the pure myxoid (0% of RC component) and RC with high cellular component (≥80%).

2014-10-30 | GSE55464 | GEO

Gene expression profiling of myxoid liposarcomas (validation set INT-B)

2014-10-30 | GSE55465 | GEO

Gene expression profiling of myxoid liposarcomas (validation set INT-B)

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Mechanisms associated with systemic effects of cancer

Project description:Cancer is considered as a disease of a specific organ, but its effects are felt throughout the body. The systemic effects of cancer can lead to weakness in muscles and heart, which hastens cancer-associated death. miR-486 is a myogenic microRNA and its reduced expression in skeletal muscle is observed in muscular dystrophy. Muscle-specific transgenic expression of miR-486 using muscle creatine kinase promoter (MCK-miR-486) partially rescues skeletal muscle defects in muscular dystrophy animal models. We had previously demonstrated reduced circulating and skeletal muscle levels of miR-486 in several cancer types and lower miR-486 levels correlated with skeletal muscle defects and functional limitations in mammary tumor models. Therefore, skeletal muscle defects induced by cancer could resemble defects observed in various dystrophies, which could be reversed through skeletal muscle expression of miR-486. We performed functional limitations studies and biochemical analysis of skeletal muscles of MMTV-Neu transgenic mice that mimic HER2+ breast cancer and MMTV-PyMT transgenic mice that mimic luminal subtype B breast cancer and these mice crossed to MCK-miR-486 transgenic mice. miR-486 significantly prevented tumor-induced reduction in muscle contraction force, grip strength, and rotarod performance in MMTV-Neu, but not in MMTV-PyMT mice. In MMTV-Neu model, miR-486 reversed several of the cancer-induced changes in skeletal muscle including loss of p53, phospho-AKT, and phospho-laminin alpha 2 (LAMA2) and gain of phosphorylation of the pre-mRNA processing factor hnRNPA0 and the splicing factor SRSF10. LAMA2 is a part of the dystrophin-associated glycoprotein complex, and its loss-of-function mutation is associated with congenital muscular dystrophy. Thus, similar to muscular dystrophy, miR-486 has the potential to reverse skeletal muscle defects and cancer burden in select cancer types.

2022-05-19 | PXD028554 | Pride

Myxoid liposarcoma tumor gene expression by array analysis

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