A novel oncogenic pathway by TLS–CHOP involving repression of MDA-7/IL-24 expression

BACKGROUND: Translocated in liposarcoma-CCAAT/enhancer binding protein homologous protein (TLS–CHOP) (also known as FUS-DDIT3) chimeric oncoprotein is found in the majority of human myxoid liposarcoma (MLS), but its molecular function remains unclear. METHODS: We knockdowned TLS–CHOP expression in M...

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Detalles Bibliográficos
Autores principales: Oikawa, K, Tanaka, M, Itoh, S, Takanashi, M, Ozaki, T, Muragaki, Y, Kuroda, M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2012
Materias:
Short Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3388565/
https://www.ncbi.nlm.nih.gov/pubmed/22588557
http://dx.doi.org/10.1038/bjc.2012.199
Descripción
Sumario:BACKGROUND: Translocated in liposarcoma-CCAAT/enhancer binding protein homologous protein (TLS–CHOP) (also known as FUS-DDIT3) chimeric oncoprotein is found in the majority of human myxoid liposarcoma (MLS), but its molecular function remains unclear. METHODS: We knockdowned TLS–CHOP expression in MLS-derived cell lines by a specific small interfering RNA, and analysed the gene expression profiles with microarray. RESULTS: TLS-CHOP knockdown inhibited growth of MLS cells, and induced an anticancer cytokine, melanoma differentiation-associated gene 7 (MDA-7)/interleukin-24 (IL-24) expression. However, double knockdown of TLS–CHOP and MDA-7/IL-24 did not inhibit MLS cell growth. CONCLUSION: Repression of MDA-7/IL-24 expression by TLS–CHOP is required for MLS tumour growth, and TLS–CHOP may become a promising therapeutic target for MLS treatment.

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