Oncogenic Role of Skp2 and p27^Kip1 in Intraductal Proliferative Lesions of the Breast

• Published in: 中国医学科学杂志：英文版 Vol. 27; no. 3; pp. 161 - 166
• Main Author: Yan Lv Yun Niu Xiu-min Ding Xu-qi Xiao
• Format: Journal Article
• Language: English
• Published: 2012
• Subjects: p27; Skp2; 乳腺癌; 增生性; 病变; 石蜡包埋组织; 管内; 致癌作用
• ISSN: 1001-9294

Objective To investigate whether the connection of p27^Kip1 to S-phase kinase-associated protein 2 （Skp2） plays an oncogenic role in intraductal proliferative lesions of the breast. Methods Here we investigated the mechanism involved in association of Skp2’s degradation of p27^Kip1 with the breast carcinogenesis by immunohistochemical method through detection of Skp2 and p27^Kip1 protein levels in 120 paraffin-embedded tissues of intraductal proliferative lesions including usual ductal hyperplasia （UDH, n=30）, atypical ductal hyperplasia （n=30）, flat epithelial atypia （FEA, n=30）, and ductal carcinoma in situ （DCIS, n=30）. Moreover, the expression status of Skp2 and p27^Kip1 in 30 cases of the normal breast paraffin-embedded tissues were explored. Results The DCIS group was with the highest Skp2 level and the lowest p27^Kip1 level, and the UDH group was with the lowest Skp2 level and the highest p27^Kip1 level. Both Skp2 and p27^Kip1 levels in the DCIS group were significantly different from those in the UDH group （all P〈0.01）. The levels of Skp2 and p27^Kip1 in the FEA group were significantly different from both the DCIS and UDH groups （all P〈0.05）. p27^Kip1 was negatively correlated with Skp2 in both the UDH group （r=-0.629, P=0.026） and DCIS group （r=-0.893, P=0.000）. Conclusion Overexpression of Skp2 might be the mechanism underlying p27^Kip1 over degradation.