Abstract: To explore the possible roles of NGX6, ILK, and c-Jun in the carcinogenesis of sporadic colorectal tubular adenoma. Methods: The expression levels of NGX6, ILK, and c-Jun were studied in 22 cases of dysplastic aberrant crypt foci ( ACF ), 68 cases of sporadic colorectal tubular adenoma with dysplasia ( SCTA-D ), 21 cases of sporadic colorectal tubular adenoma with cancerous changes ( SCTA-Ca ), and 21 cases of normal control ( NC ) by the immunohistochemical staining method. Results: The positive expression rate of NGX6 significantly decreased from NC, dysplastic ACF, and SCTA-D to SCTA-Ca. In contrast, the positive expression rates of ILK and c-Jun obviously increased accordingly ( P < 0.05 ). The positive expression rates of NGX6 in dysplastic ACF, mild SCTA-D, moderate SCTA-D, and severe SCTA-D were 77.27%, 70.83%, 37.50%, and 35.00%, respectively. Compared with that of dysplastic ACF or mild SCTA-D, the positive expression rates of NGX6 in moderate and severe SCTA-D significantly decreased ( P < 0.05 ). In severe SCTA-D, ILK expression was also significantly higher than those in dysplastic ACF, mild SCTA-D, and moderate SCTA-D ( P < 0.05 ). The positive expression rates of c-Jun in both SCTA-D and SCTA-Ca were significantly higher as well than that in dysplastic ACF ( P < 0.05 ). In the carcinogenic process of sporadic colorectal tubular adenoma, a negative correlation was found between the expression of NGX6 and ILK ( r = -0.455, P < 0.05 ), as well as between NGX6 and c-Jun ( r = -0.417, P < 0.05 ). On the other hand, a positive correlation was found between the expression levels of ILK and c-Jun ( r = 0.390, P < 0.05 ). Conclusion: The down-regulation of NGX6 as well as the up-regulation of ILK and c-Jun may play important roles in colorectal adenoma formation and carcinogenesis.