HOXB13 promotes proliferation, migration, and invasion of glioblastoma through transcriptional upregulation of lncRNA HOXC‐AS3
HOXB13 exerts a close relation in several human cancers. This study explored the role of HOXB13 in glioblastoma (GBM), a brain tissue with the highest aggressive rate and mortality in adults. Through microarray and immunohistochemistry analyses, HOXB13 was highly expressed in GBM tissues. Furthermor...
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Published in | Journal of cellular biochemistry Vol. 120; no. 9; pp. 15527 - 15537 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Wiley Subscription Services, Inc
01.09.2019
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Subjects | |
Online Access | Get full text |
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Summary: | HOXB13 exerts a close relation in several human cancers. This study explored the role of HOXB13 in glioblastoma (GBM), a brain tissue with the highest aggressive rate and mortality in adults. Through microarray and immunohistochemistry analyses, HOXB13 was highly expressed in GBM tissues. Furthermore, we showed that high‐level expression of HOXB13 in GBM was associated with worse survival, suggesting that HOXB13 could be a prognostic marker for patients with GBM. GBM cells U87 and U251 overexpressing HOXB13 showed enhanced proliferation, migration, and invasion relative to the control cells, while knockdown of HOXB13 led to decreased cell proliferation, migration, and invasion abilities. In addition, dual‐luciferase report assay, chromatin immunoprecipitation assay, and quantitative real‐time polymerase chain reaction data showed that HOXB13 directly bound to HOXC‐AS3 promoter. HOXC‐AS3 was involved in HOXB13‐induced proliferation, migration, and invasion of GBM cells. In summary, this study revealed the prognostic potential of HOXB13 in GBM. We believed that HOXB13/HOXC‐AS3 signaling axis can be served as therapeutic targets for this highly aggressive cancer.
HOXB13, was overexpressed in glioblastoma (GBM) tissues. Overexpression of HOXB13 enhanced cell growth and promoted GBM cells to migrate and invade through upregulating HOXC‐AS3. |
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Bibliography: | Wang and Sun have contributed equally to this study. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0730-2312 1097-4644 |
DOI: | 10.1002/jcb.28819 |