Both the morphogenesis and the molecular pathways of thyroid cancers are controversial. Programmed cell death 4 (PDCD4) is a tumor suppressor gene whose expression is controlled by miR-21. By applying immunohistochemistry for PDCD4 and both quantitative real-time PCR (qRT-PCR) and in situ hybridization formiR-21, this study explored PDCD4 expression in human follicular-cell-derived thyroid neoplastic lesions. PDCD4 protein expression was semiquantitatively assessed in 100 consecutive thyroid tumors (25 follicular adenomas (FA), 25 follicular carcinomas (FC), 25 papillary carcinomas (PC), and 25 poorly-differentiated/anaplastic cancers (PD-AC)). Twenty-five additional nonneoplastic thyroid tissue samples were included as controls. To further support the data, miR-21 expression was tested (by qRT-PCR and in situ hybridization) in a different series of 75 cases (15 FAs, 15 FCs, 15 PCs, 15 PD-ACs, and 15 controls). Nonneoplastic thyrocytes consistently featured a strong nuclear PDCD4 expression, while the protein's expression was significantly downregulated in neoplastic epithelia. PDCD4 downregulation was significantly associated with less well-differentiated cancer phenotypes (p<0.001) and more advanced tumor stages (p<0.001). Consistently with PDCD4 downregulation, miR-21 was upregulated in neoplastic by comparison with nonneoplastic tissue samples. The present results provide evidence of PDCD4 having a role in thyroid carcinogenesis; further studies should investigate the diagnostic value and the prognostic impact of PDCD4 in thyroid neoplasia. Keywords

PDCD4 expression in thyroid neoplasia

PENNELLI, GIANMARIA;FASSAN, MATTEO;MIAN, CATERINA;PIZZI M;BAROLLO, SUSI;GALUPPINI F;PELIZZO, MARIA ROSA;RUGGE, MASSIMO
2013

Abstract

Both the morphogenesis and the molecular pathways of thyroid cancers are controversial. Programmed cell death 4 (PDCD4) is a tumor suppressor gene whose expression is controlled by miR-21. By applying immunohistochemistry for PDCD4 and both quantitative real-time PCR (qRT-PCR) and in situ hybridization formiR-21, this study explored PDCD4 expression in human follicular-cell-derived thyroid neoplastic lesions. PDCD4 protein expression was semiquantitatively assessed in 100 consecutive thyroid tumors (25 follicular adenomas (FA), 25 follicular carcinomas (FC), 25 papillary carcinomas (PC), and 25 poorly-differentiated/anaplastic cancers (PD-AC)). Twenty-five additional nonneoplastic thyroid tissue samples were included as controls. To further support the data, miR-21 expression was tested (by qRT-PCR and in situ hybridization) in a different series of 75 cases (15 FAs, 15 FCs, 15 PCs, 15 PD-ACs, and 15 controls). Nonneoplastic thyrocytes consistently featured a strong nuclear PDCD4 expression, while the protein's expression was significantly downregulated in neoplastic epithelia. PDCD4 downregulation was significantly associated with less well-differentiated cancer phenotypes (p<0.001) and more advanced tumor stages (p<0.001). Consistently with PDCD4 downregulation, miR-21 was upregulated in neoplastic by comparison with nonneoplastic tissue samples. The present results provide evidence of PDCD4 having a role in thyroid carcinogenesis; further studies should investigate the diagnostic value and the prognostic impact of PDCD4 in thyroid neoplasia. Keywords
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3029157
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