Molecular signature induced by RNASET2, a tumor antagonizing gene, in ovarian cancer cells
Metrics: PDF 1619 views | HTML 1932 views | ?
1 Dipartimento di Biotecnologie e Scienze Molecolari, Università degli Studi dell'Insubria, via JH Dunant 3, 21100 Varese, Italy
2 European Commission - Joint Research Centre Institute for Health and Consumer Protection Molecular Biology and Genomics unit TP 464, Via E. Fermi, 2749 21027 Ispra (VA) - Italy
Keywords: RNases, cancer microenvironment, transcriptional profile
Received: May 10, 2011; Accepted: June 2, 2011; Published: June 4, 2011;
Roberto Taramelli, e-mail:
Francesco Acquati, e-mail:
As previously reported, using the Hey3Met2 human ovarian cancer cell line as an experimental model, we found the RNASET2 gene to possess a remarkable in vivo tumor suppressor activity, although no in vitro features such as inhibition of cell proliferation, clonogenic potential, impaired growth in soft agar and increase in apoptotic rate could be detected. This is reminiscent of the behaviour of genes belonging to the class of tumor antagonizing genes (TAG) which are supposed to act mainly within the context of the microenvironment. Although the principal function of RNASET2 is non cell autonomous, more cell centered effects could not be ruled out at the present time. To such goal we have carried out transcriptional profiles analysis which indicated, on one hand, that investigations of the mechanisms through which TAG carry out their biological functions require a thorough comparison between the in vitro and in vivo expression patterns. Indeed several genes displaying a biological function potentially related to tumor suppression could not be validated by subsequent in vivo expression analysis. On the other hand the fact that we could find congruency for three genes both in vivo and in vitro adds a warning to a too much stringent categorisation of this class of genes which relies on the sensitivity of the methodological approach undertaken.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.