Influence of IFN-gamma and its receptors in human breast cancer
AuthorsGarcía Tuñón Llanio, Ignacio; Ricote Belinchón, Mónica; Ruiz A., Antonio; Fraile Laiz, Benito; Paniagua Gómez-Álvarez, Ricardo; [et al.]
IdentifiersPermanent link (URI): http://hdl.handle.net/10017/5918
BMC Cancer, 2007, v. 7, p. 158
Atribución-NoComercial-SinDerivadas 3.0 España
© García-Tuñón et al; licensee BioMed Central Ltd., 2007
Interferons are a group of proteins that trigger multiple responses including prevention of viral replication, inhibition of cell growth, and modulation of cell differentiation. In different mammary carcinoma cell lines IFNÎ³ induces growth arrest at mid-G1. At the present there are no in vivo studies in human breast. The aim of this study was to investigate the expression patterns of IFNÎ³ and its two receptors (IFNÎ³-RÎ± and IFNÎ³-RÎ²) by Western blot and immunohistochem., in order to elucidate its role in the different types of human breast cancer (in situ and infiltrative). Methods: Immunohistochem. and semiquant. study of IFNÎ³, its receptors types (IFNÎ³-RÎ± and IFNÎ³-RÎ²), cell proliferation (proliferating cell nuclear antigen, also named PCNA), and apoptosis (Tunel method) was carried between the three breast groups (fibrocystic lesions, in situ tumors and infiltrating tumors). Results: In the three groups of patients, IFNÎ³ and IFNÎ³-RÎ± immunoreactions appeared in the cytoplasm while IFNÎ³-RÎ² also was found in the nucleus. The optical d. of IFNÎ³ was higher in in situ carcinoma than in benign and infiltrating tumors. When we obsd. IFNÎ³-RÎ±, the optical d. was lower in infiltrating carcinoma than in benign and in situ tumors (the higher d.). To IFNÎ³-RÎ², the optical d. was similar in the three group samples. In tumor samples PCNA and TUNEL index was significantly higher; than in benign diseases. PCNA index increased with the malignance. No significant differences were found between cancer types to TUNEL. IFNÎ³ could be a potential therapeutic tool in breast cancer. However, tumor cells are able to escape from the control of this cytokine in the early tumor stages; this is probably due to a decreased expression of IFNÎ³, or also to an alteration of either its receptors or some transduction elements. Conclusions: We conclude that the decrease in the % pos. samples that expressed IFNÎ³ and IFNÎ³-RÎ± together with the nuclear localization of IFNÎ³-RÎ², could be a tumoral cell response, although perhaps insufficient to inhibit the uncontrolled cell proliferation. Perhaps, IFNÎ³ might be unable to activate p21 to stop the cell cycle, suggesting a possible participation in breast cancer development.