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Mol Cell Endocrinol. 2016 May 5;426:22-32. doi: 10.1016/j.mce.2016.02.009. Epub 2016 Feb 15.

Evidence for possible role of toll-like receptor 3 mediating virus-induced progression of pituitary adenomas.

Author information

1
Multidisciplinary Center for Pituitary Adenomas of Chongqing, Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China.
2
Innovative Drug Research Centre, University of Chongqing, China.
3
Department of Biology and Biochemistry, College of Natural Sciences and Mathematics, University of Houston, TX, USA. Electronic address: wzhang13@uh.edu.
4
Multidisciplinary Center for Pituitary Adenomas of Chongqing, Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China. Electronic address: yanghui64@hotmail.com.

Abstract

Tumor-related viruses are known to be involved in initiation and progression of certain tumors. However, the relationship between virus and pituitary adenomas (PAs) remains unknown. Here, we investigated infection status of three types of viruses (HPV16, HHV6B and HSV1) and expression level of toll-like receptor 3 (TLR3) in 60 human PA samples. We also determined the role of TLR3 signaling pathway on a PA cell line (GH3). We firstly found that positive rates of HPV16 and HHV6B infection were significantly higher in invasive PA samples than in noninvasive samples (P < 0.01). Similarly, TLR3 mRNA and protein expression also increased in invasive PA samples (P < 0.01). In vitro analysis indicated that GH3 cell proliferation and survival were enhanced by TLR3 activation, which was accompanied by NF-κB activation. Our data indicate that HPV16 and HHV6B viruses may be involved in promoting the progression of PA by activating the TLR3 signaling pathway.

KEYWORDS:

Pituitary adenoma; Progression; Toll-like receptor 3; Viruses

PMID:
26891958
DOI:
10.1016/j.mce.2016.02.009
[Indexed for MEDLINE]

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