Context: The ability of tumor cells to invade adjacent tissues is governed by a complicated network of molecular signals, most of which have not yet been identified. In a recent work, we reported that the transcriptional regulator Id1 contributes to thyroid cancer progression by powering the invasion capacity of tumor cells. Objective: The intent of this work was to further investigate the biology of invasive thyroid tumors, through the analysis of the molecular interactions existing between Id1 and some of its target genes and through the characterization of the function of these factors in the progression of thyroid tumors. Results: We showed that Id1 controls the expression of the Runx2 isoform I and that this transcription factor plays a central role in mediating the Id1 proinvasive function in thyroid tumor cells. We demonstrated that Runx2 regulates proliferation, migration, and invasiveness by activating a panel of genes involved in matrix degradation and cellular invasion, which we previously identified as Id1 target genes in thyroid tumor cells. Finally, we show that Runx2 is strongly expressed in metastatic human thyroid tumors both at the primary site and in metastases. Conclusion: Overall, our experiments demonstrate the existence of a previously unknown molecular axis that controls thyroid tumor invasiveness by altering the ability of tumor cells to interact with the surrounding microenvironment. These factors could prove to be valuable markers that permit early diagnosis of aggressive thyroid tumors. (J Clin Endocrinol Metab 97: E2006-E2015, 2012)

Runx2 Isoform I Controls a Panel of Proinvasive Genes Driving Aggressiveness of Papillary Thyroid Carcinomas / Sancisi, V; Borettini, G; Maramotti, S; Ragazzi, M; Tamagnini, I; Nicoli, D; Piana, S; Ciarrocchi, A. - In: THE JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM. - ISSN 0021-972X. - 97:10(2012), pp. E2006-E2015. [10.1210/jc.2012-1903]

Runx2 Isoform I Controls a Panel of Proinvasive Genes Driving Aggressiveness of Papillary Thyroid Carcinomas

Ragazzi M;
2012

Abstract

Context: The ability of tumor cells to invade adjacent tissues is governed by a complicated network of molecular signals, most of which have not yet been identified. In a recent work, we reported that the transcriptional regulator Id1 contributes to thyroid cancer progression by powering the invasion capacity of tumor cells. Objective: The intent of this work was to further investigate the biology of invasive thyroid tumors, through the analysis of the molecular interactions existing between Id1 and some of its target genes and through the characterization of the function of these factors in the progression of thyroid tumors. Results: We showed that Id1 controls the expression of the Runx2 isoform I and that this transcription factor plays a central role in mediating the Id1 proinvasive function in thyroid tumor cells. We demonstrated that Runx2 regulates proliferation, migration, and invasiveness by activating a panel of genes involved in matrix degradation and cellular invasion, which we previously identified as Id1 target genes in thyroid tumor cells. Finally, we show that Runx2 is strongly expressed in metastatic human thyroid tumors both at the primary site and in metastases. Conclusion: Overall, our experiments demonstrate the existence of a previously unknown molecular axis that controls thyroid tumor invasiveness by altering the ability of tumor cells to interact with the surrounding microenvironment. These factors could prove to be valuable markers that permit early diagnosis of aggressive thyroid tumors. (J Clin Endocrinol Metab 97: E2006-E2015, 2012)
2012
97
10
E2006
E2015
Runx2 Isoform I Controls a Panel of Proinvasive Genes Driving Aggressiveness of Papillary Thyroid Carcinomas / Sancisi, V; Borettini, G; Maramotti, S; Ragazzi, M; Tamagnini, I; Nicoli, D; Piana, S; Ciarrocchi, A. - In: THE JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM. - ISSN 0021-972X. - 97:10(2012), pp. E2006-E2015. [10.1210/jc.2012-1903]
Sancisi, V; Borettini, G; Maramotti, S; Ragazzi, M; Tamagnini, I; Nicoli, D; Piana, S; Ciarrocchi, A
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/1302290
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