RESUMO
<p><b>OBJECTIVE</b>To study the possible role of JNK1, Raf-1 and Livin in the carcinogenesis of sporadic colorectal tubular adenoma.</p><p><b>METHODS</b>Immunohistochemical staining was used to detect the expression of JNK1, Raf-1 and Livin proteins in 65 sporadic colorectal tubular adenomas with dysplasia of varying degrees and 22 colorectal tubular adenoma with cancerous area.</p><p><b>RESULTS</b>In normal colorectal mucosa, colorectal tubular adenoma with dysplasia and colorectal tubular adenoma with cancerous area, the positive rate of JNK1, Raf-1 and Livin expression was increased gradually. The positive expression of JNK1, Raf-1 and Livin was all significantly higher in the cases of colorectal tubular adenoma with dysplasia or with cancerous area than that in normal colorectal mucosa (P < 0.05), and the positive expression of JNK1, Raf-1 and Livin was significantly higher in colorectal tubular adenoma with cancerous area than that in colorectal tubular adenoma with dysplasia of different degrees (P < 0.05). In the cases of colorectal tubular adenoma with dysplasia of varying degrees, the positive expression of Raf-1 was increased along with the increasing dysplasia degree of colorectal tubular adenoma (P < 0.05). Coexpression of JNK1, Raf-1 and Livin increased gradually in the carcinogenesis of sporadic colorectal tubular adenoma, while positive correlation was found among the expressions of JNK1, Raf-1 and Livin.</p><p><b>CONCLUSION</b>JNK1, Raf-1 and Livin may be involved in the carcinogenesis of sporadic colorectal tubular adenoma.</p>
Assuntos
Adulto , Feminino , Humanos , Masculino , Proteínas Adaptadoras de Transdução de Sinal , Metabolismo , Adenoma , Metabolismo , Patologia , Carcinoma , Metabolismo , Patologia , Transformação Celular Neoplásica , Neoplasias Colorretais , Metabolismo , Patologia , Proteínas Inibidoras de Apoptose , Metabolismo , Mucosa Intestinal , Metabolismo , Patologia , Proteína Quinase 8 Ativada por Mitógeno , Metabolismo , Proteínas de Neoplasias , Metabolismo , Lesões Pré-Cancerosas , Metabolismo , Patologia , Proteínas Proto-Oncogênicas c-raf , MetabolismoRESUMO
<p><b>OBJECTIVE</b>To investigate the possible role of STAT3 and p38 in the carcinogenesis of sporadic colorectal tubular adenoma.</p><p><b>METHODS</b>The expression of STAT3 and p38 at protein level was studied in 107 sporadic colorectal tubular adenomas with different dysplasia (SCTA-D) or with cancerous changes (SCTA-Ca) by immunohistochemical staining method, meanwhile the expression of STAT3 at mRNA level was detected by in situ hybridization.</p><p><b>RESULTS</b>Immunohistochemical staining results showed that the positive expression rate of STAT3 and p38 was 12.0%, 59.0%, 91.7% and 8.0%, 47.0%, 91.7% in normal colorectal mucosa (NCM), SCTA-D and SCTA-Ca, respectively, with a statistically significant difference of STAT3 and p38 expression among the SCTA-D, SCTA-Ca and NCM (P < 0.05). The expression of STAT3 and p38 was positively correlated with the degree of dysplasia from mild to severe SCTA-D (P < 0.05). In situ hybridization results showed that the positive expression rate of STAT3 at mRNA level in NCM, SCTA-D and SCTA-Ca was 8.00%, 51.8% and 100.0%, respectively, with a statistically significant difference among these either (P < 0.05). The positive expression of STAT3 at mRNA level was not only positively correlated with the degree of dysplasia (P < 0.05), but also with the expression of p38 (P < 0.05).</p><p><b>CONCLUSION</b>STAT3 and p38 may be involved in the carcinogenesis of sporadic colorectal tubular adenoma.</p>