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10.1186/s12943-018-0846-5 http://scihub22266oqcxt.onion/10.1186/s12943-018-0846-5 C6047127!6047127 !30008265     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30008265 &cmd=llinks): Failed to open stream: HTTP request failed! 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Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation |pdf=|usr=}}{{30008265 }} gab.com Text Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation JO: Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=30008265 #FOAvip BACKGROUND: Exosomes are extracellular vesicles released by almost all cell types, including cancer cells, into bodily fluids such as saliva, plasma, breast milk, semen, urine, cerebrospinal fluid, amniotic fluid, synovial fluid and sputum. Their key function being intercellular communication with both neighbouring as well as distant cells. Cancer exosomes have been shown to regulate organ-specific metastasis. However, little is known about the functional differences and molecular consequences of normal cells responding to exosomes derived from normal cells compared to those derived from cancer cells. METHODS: Here, we characterised and compared the transcriptome profiles of primary human normal oral keratinocytes (HNOK) in response to exosomes isolated from either primary HNOK or head and neck squamous cell carcinoma (HNSCC) cell lines. RESULTS: In recipient HNOK cells, we found that regardless of normal or cancer derived, exosomes altered molecular programmes involved in matrix modulation (MMP9), cytoskeletal remodelling (TUBB6, FEZ1, CCT6A), viral/dsRNA-induced interferon (OAS1, IFI6), anti-inflammatory (TSC22D3), deubiquitin (OTUD1), lipid metabolism and membrane trafficking (BBOX1, LRP11, RAB6A). Interestingly, cancer exosomes, but not normal exosomes, modulated expression of matrix remodelling (EFEMP1, DDK3, SPARC), cell cycle (EEF2K), membrane remodelling (LAMP2, SRPX), differentiation (SPRR2E), apoptosis (CTSC), transcription/translation (KLF6, PUS7). We have also identified CEP55 as a potential cancer exosomal marker. CONCLUSIONS: In conclusion, both normal and cancer exosomes modulated unique gene expression pathways in normal recipient cells. Cancer cells may exploit exosomes to confer transcriptome reprogramming that leads to cancer-associated pathologies such as angiogenesis, immune evasion/modulation, cell fate alteration and metastasis. Molecular pathways and biomarkers identified in this study may be clinically exploitable for developing novel liquid-biopsy based diagnostics and immunotherapies. Twit Text FOAVip Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation ????Mol Cancer http://www.kidney.de/pget.php?&tw=1&pmid=30008265 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30008265 #FOAvip English Wikipedia <ref>{{Cite pmid|30008265 }}</ref> Transcriptome reprogramming by cancer exosomes: identification of novel molecular targets in matrix and immune modulation #MMPMID30008265 Qadir F ; Aziz MA ; Sari CP ; Ma H ; Dai H ; Wang X ; Raithatha D ; Da Silva LGL ; Hussain M ; Poorkasreiy SP ; Hutchison IL ; Waseem A ; Teh MT Mol Cancer 2018[Jul]; 17 (1 ): 97 PMID30008265 show ga BACKGROUND: Exosomes are extracellular vesicles released by almost all cell types, including cancer cells, into bodily fluids such as saliva, plasma, breast milk, semen, urine, cerebrospinal fluid, amniotic fluid, synovial fluid and sputum. Their key function being intercellular communication with both neighbouring as well as distant cells. Cancer exosomes have been shown to regulate organ-specific metastasis. However, little is known about the functional differences and molecular consequences of normal cells responding to exosomes derived from normal cells compared to those derived from cancer cells. METHODS: Here, we characterised and compared the transcriptome profiles of primary human normal oral keratinocytes (HNOK) in response to exosomes isolated from either primary HNOK or head and neck squamous cell carcinoma (HNSCC) cell lines. RESULTS: In recipient HNOK cells, we found that regardless of normal or cancer derived, exosomes altered molecular programmes involved in matrix modulation (MMP9), cytoskeletal remodelling (TUBB6, FEZ1, CCT6A), viral/dsRNA-induced interferon (OAS1, IFI6), anti-inflammatory (TSC22D3), deubiquitin (OTUD1), lipid metabolism and membrane trafficking (BBOX1, LRP11, RAB6A). Interestingly, cancer exosomes, but not normal exosomes, modulated expression of matrix remodelling (EFEMP1, DDK3, SPARC), cell cycle (EEF2K), membrane remodelling (LAMP2, SRPX), differentiation (SPRR2E), apoptosis (CTSC), transcription/translation (KLF6, PUS7). We have also identified CEP55 as a potential cancer exosomal marker. CONCLUSIONS: In conclusion, both normal and cancer exosomes modulated unique gene expression pathways in normal recipient cells. Cancer cells may exploit exosomes to confer transcriptome reprogramming that leads to cancer-associated pathologies such as angiogenesis, immune evasion/modulation, cell fate alteration and metastasis. Molecular pathways and biomarkers identified in this study may be clinically exploitable for developing novel liquid-biopsy based diagnostics and immunotherapies. |Biomarkers, Tumor/genetics [MESH] |Cell Cycle Proteins/*genetics [MESH] |Cell Line, Tumor [MESH] |Exosomes/*genetics/pathology [MESH] |Forkhead Box Protein M1/genetics [MESH] |Gene Expression Profiling/*methods [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Head and Neck Neoplasms/*genetics/pathology [MESH] |Humans [MESH] |Keratinocytes/cytology/metabolism/pathology [MESH] |Nuclear Proteins/*genetics [MESH] |Oligonucleotide Array Sequence Analysis/methods [MESH]Transcriptome reprogramming by cancer exosomes: identification of nove(epmc).pdf DeepDyve Pubget Overpricing