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Pituitary adenoma xenografts were generated in immunocompromised mice.
ASA decreased proliferation but did not induce apoptosis in pituitary cells. Inhibition of survivin using an inhibitor or siRNA-mediated silencing reversed the ASA-induced growth inhibition partially. We concluded that ASA inhibited the growth of pituitary adenoma cells.
Survivin inhibition is a key mechanism explaining its antineoplastic effects. Beside cell cycle alterations, inhibition of apoptosis is also a potential mechanism leading to tumorigenesis in pituitary adenomas.
Proteomic studies also suggest deranged apoptosis in pituitary adenomas [ 7 ]. Survivin, a member of inhibitor of apoptosis protein IAP family, plays a role in both apoptosis inhibition and cell cycle regulation, although the mechanism of its action has not been clarified. Elevated survivin expression is present in a variety of cancers [ 8 ] and its expression correlates with aggressiveness and poor survival [ 910 ].
Thus, survivin is considered as a potential target in cancer therapies [ 11 ]. However, little is known about the role of survivin in pituitary tumors.
In a recent paper published while our prostate size normal values was in final preparations, the authors showed that survivin associated with invasiveness of pituitary adenomas [ 1012 ]. As survivin is suppressed by acetylsalicylic acid ASAan agent used as chemoprevention for colorectal cancer [ 1314 ], we studied the therapeutic potential of ASA in pituitary tumours, and assess its potential effects on survivin.
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We hypothesized that ASA might affect various cellular processes through survivin, that could lead to reduced growth and beneficial overall effects. Now, we extended this study to GH-producing adenomas with 12 samples and we found that survivin mRNA was overexpressed compared to normal pituitary fold change: 4.
No cytoplasmic staining was observed.
Analyzing moderate and strong positivity we found that