Journal
GENES
Volume 13, Issue 4, Pages -Publisher
MDPI
DOI: 10.3390/genes13040674
Keywords
connexins; pituitary neuroendocrine tumors; apoptosis
Categories
Funding
- Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro [APQ1 E-26/111.972/2012, JCNE FAPERJ/2014, E-26/201.520/2014]
- Conselho Nacional de Desenvolvimento Cientifico (CNPq)
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES/Ciencias sem Fronteiras/Pesquisador Visitante Especial) [88881.062218/2014-0]
- project Cancer Research on Therapy Resistance: From Basic Mechanisms to Novel Targets [NORTE-01-0145-FEDER-000051]
- Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF)
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Gap junction intercellular communication (GJIC) and connexin protein expression alterations are related to the tumorigenesis and potential therapeutic value of pituitary neuroendocrine tumors (PitNETs), particularly the downregulation of Cx43 protein.
Gap junction intercellular communication (GJIC) is considered a key mechanism in the regulation of tissue homeostasis. GJIC structures are organized in two transmembrane channels, with each channel formed by connexins (Cxs). GJIC and Cxs expression alterations are related to the process of tumorigenesis in different cell types. Pituitary neuroendocrine tumors (PitNETs) represent 15-20% of intracranial neoplasms, and usually display benign behavior. Nevertheless, some may have aggressive behavior, invading adjacent tissues, and featuring a high proliferation rate. We aimed to assess the expression and relevance of GJIC and Cxs proteins in PitNETs. We evaluated the mRNA expression levels of Cx26, 32, and 43, and the protein expression of Cx43 in a series of PitNETs. In addition, we overexpressed Cx43 in pituitary tumor cell lines. At the mRNA level, we observed variable expression of all the connexins in the tumor samples. Cx43 protein expression was absent in most of the pituitary tumor samples that were studied. Moreover, in vitro studies revealed that the overexpression of Cx43 decreases cell growth and induces apoptosis in pituitary tumor cell lines. Our results indicate that the downregulation of Cx43 protein might be involved in the tumorigenesis of most pituitary adenomas and have a potential therapeutic value for pituitary tumor therapy.
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