Expressions of miR-30c and let-7a are inversely correlated with HMGA2 expression in squamous cell carcinoma of the vulva
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Antonio Agostini1,2, Marta Brunetti1,2, Ben Davidson3,4, Claes G. Trope5, Sverre Heim1,2,4, Ioannis Panagopoulos1,2, Francesca Micci1,2
1Section for Cancer Cytogenetics, Institute for Cancer Genetics and Informatics, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
2Centre for Cancer Biomedicine, University of Oslo, Oslo, Norway
3Department of Pathology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
4Faculty of Medicine, University of Oslo, Oslo, Norway
5Department of Gynecology, The Norwegian Radium Hospital, Oslo University Hospital, Oslo, Norway
Francesca Micci, email: [email protected]
Keywords: HMGA2, miR-30c, let-7a, FHIT
Received: September 14, 2016 Accepted: October 22, 2016 Published: November 07, 2016
Malignant tumors of the vulva, most of them squamous cell carcinomas, account for only 5% of cancers of the female genital tract. Though little is known about the genetic features of these tumors, the Fragile Histidine Triad (FHIT) and High Mobility Group AT-hook 2 (HMGA2) genes were found deregulated. We wanted to gain more knowledge about the expression of HMGA2-related miRNAs such as miR-30c and let-7a, and whether a correlation exists between the expression of FHIT and HMGA2, in this tumor type. An inverse correlation was found in-as-much as HMGA2 was highly expressed (mean fold change 8.8) whereas miR30c and let-7a were both downregulated (mean fold change -3.9 and -2.3, respectively). The consistent overexpression of HMGA2 found in all tumors adds to the likelihood that this gene is of importance in SCC pathogenesis. Moreover, we came to the conclusion that miRNAs may be the cause of the deregulation of HMGA2. Our results also show that SCC of the vulva presents a characteristic molecular pattern with FHIT being downregulated whereas HMGA2 is upregulated.
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