期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 436, 期 C, 页码 195-203出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2016.07.025
关键词
Pituitary adenomas; Null cell adenomas; Invasion; IL-6R; JAK2; STAT3
资金
- Research Special Fund for Public Welfare Industry of Health [201402008]
- National High Technology Research and Development Program of China (863 Program) [2014AA020610]
- National Natural Science Foundation of China [81271627]
Non-functioning pituitary adenomas (NFPAs) are a highly heterogeneous group, but few studies have explored the invasion mechanism of specific subtypes of NFPAs. The objective of this study was to investigate the differential molecular expression patterns and the critical biological signaling pathways involved in the invasion of pituitary null cell adenomas (PNCAs) through integrative proteomics and transcriptomics. A total of 1160 genes and 283 proteins were found to be differentially expressed in invasive and non-invasive PNCAs. The differentially expressed molecules related to invasion were enriched in 15 canonical signaling pathways, 15 clusters of diseases or biological functions and 5 upstream molecules. Among them, the majority of the differentially expressed molecules were found to be involved in transport of molecule, migration of cells and cell movement. Notably, IL-6 was a significantly activated upstream regulator, and the IL6R/JAK2/STAT3 cascade was found to play a critical role in acute phase response signaling, which was the most significant canonical signaling pathway. Furthermore, we validated the overexpression of IL-6R, JAK2, STAT3, p-STAT3 and MMP9 in invasive PNCAs. Our data suggest that overactivation of the IL-6R/JAK2/STAT3/MMP9 pathway is critical for the invasion of PNCAs. (C) 2016 Elsevier Ireland Ltd. All rights reserved.
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