ECE2020 Oral Communications Endocrine-related Cancer (7 abstracts)
1Alicante University General Hospital, Alicante Institute for Health and Biomedical Research, Research Laboratory, Alicante, Spain; 2Alicante University General Hospital, Alicante Institute for Health and Biomedical Research, Endocrinology Department, Alicante, Spain; 3La Fe University and Polytechnic Hospital, Endocrinology Department, Valencia, Spain; 4La Ribera Hospital, Endocrinology Departmen, Alzira, Spain; 5Albacete University Hospital Complex, Endocrinology Department, Albacete, Spain; 6Alicante University General Hospital, Alicante Institute for Health and Biomedical Research, Pathology Department, Alicante, Spain
Introduction: E2F1 regulates the expression of genes required for cell cycle progression and apoptosis. miR-17-5p regulates expression of E2F1. Both miR-17-5p and E2F1 have been described deregulated in cancer but they have been scarcely studied in human pituitary neuroendocrine tumours (PitNETs).
The aim of the present study was to find biomarkers of aggressiveness in PitNETs and report the correlation between E2F1 and miR-17-5p in the regulation of the pituitary tumorigenesis.
Methods: In this cross-sectional descriptive study, we evaluated the expression of E2F1, c-myc and two microRNAs of miR-17~92 cluster (miR-20a and miR-17-5p) by qRT-PCR in 60 human PitNET samples: 29 gonadotrophs (GT), 15 functioning somatotrophs (fST), 8 functioning corticotrophs (fCT) and 8 silent corticotrophs (sCT). Clinical, radiological and pathological data were recovered to determine the pre-operative behavior of the tumour. We defined invasiveness if the tumour invaded one of the cavernous or sphenoid sinus. We defined aggressiveness depending on the invasiveness of the tumours and the Ki-67 expression.
Results: E2F1 and c-myc demonstrated different expression in PitNETs depending on subtypes (P = 0.000 and 0.004 respectively). Specifically, GT and sCT showed overexpression of E2F1 compared to the functioning variants (fST and fCT). In the whole series, E2F1 was more expressed in invasive than in non-invasive tumours (P = 0.004). Moreover, E2F1 (P = 0.001) and miR-17-5p (P = 0.011), were overexpressed in tumours with high grade of aggressiveness in the whole series.
Conclusions: We confirm the deregulation of E2F1 and c-myc in the pathogeneis of PitNETs, with different behavior depending on their subtypes. Moreover, E2F1 and miR-17-5p could be good markers of PitNET aggressiveness.