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dc.contributor.authorHsu, Min-Kungen_US
dc.contributor.authorPan, Chia-Linen_US
dc.contributor.authorChen, Feng-Chien_US
dc.date.accessioned2019-04-03T06:44:50Z-
dc.date.available2019-04-03T06:44:50Z-
dc.date.issued2016-01-01en_US
dc.identifier.issn1178-6930en_US
dc.identifier.urihttp://dx.doi.org/10.2147/OTT.S94897en_US
dc.identifier.urihttp://hdl.handle.net/11536/133480-
dc.description.abstractIntroduction: Alternative RNA splicing is a critical regulatory mechanism during tumorigenesis. However, previous oncological studies mainly focused on the splicing of individual genes. Whether and how transcript isoforms are coordinated to affect cellular functions remain underexplored. Also of great interest is how the splicing regulome cooperates with the transcription regulome to facilitate tumorigenesis. The answers to these questions are of fundamental importance to cancer biology. Results: Here, we report a comparative study between the transcript-based network (TN) and the gene-based network (GN) derived from the transcriptomes of paired tumor-normal tissues from 77 lung adenocarcinoma patients. We demonstrate that the two networks differ significantly from each other in terms of patient clustering and the number and functions of network modules. Interestingly, the majority (89.5%) of multi-transcript genes have their transcript isoforms distributed in at least two TN modules, suggesting regulatory and functional divergences between transcript isoforms. Furthermore, TN and GN modules share only similar to 50%-60% of their biological functions. TN thus appears to constitute a regulatory layer separate from GN. Nevertheless, our results indicate that functional convergence and divergence both occur between TN and GN, implying complex interactions between the two regulatory layers. Finally, we report that the expression profiles of module members in both TN and GN shift dramatically yet concordantly during tumorigenesis. The mechanisms underlying this coordinated shifting remain unclear yet are worth further explorations. Conclusion: We show that in lung adenocarcinoma, transcript isoforms per se are coordinately regulated to conduct biological functions not conveyed by the network of genes. However, the two networks may interact closely with each other by sharing the same or related biological functions. Unraveling the effects and mechanisms of such interactions will significantly advance our understanding of this deadly disease.en_US
dc.language.isoen_USen_US
dc.subjectlung adenocarcinomaen_US
dc.subjecttranscriptome analysisen_US
dc.subjectgene networken_US
dc.subjectmoduleen_US
dc.subjectalternative splicingen_US
dc.subjecttranscriptional regulationen_US
dc.titleFunctional divergence and convergence between the transcript network and gene network in lung adenocarcinomaen_US
dc.typeArticleen_US
dc.identifier.doi10.2147/OTT.S94897en_US
dc.identifier.journalONCOTARGETS AND THERAPYen_US
dc.citation.volume9en_US
dc.citation.spage335en_US
dc.citation.epage347en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.identifier.wosnumberWOS:000368403300001en_US
dc.citation.woscount2en_US
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