Abstract 2862: Overexpression of nuclear karyopherin alpha2 correlates with poor prognosis in patients with colorectal cancer

Abstract

Abstract Objectives: Karyopherin alpha 2 (KPNA2) is a member of the karyopherin family that moves protein molecules into the nucleus by binding to a specific recognition sequence. It has recently been reported to play an important role in carcinogenesis and cancer progression. The aim of the present study was to elucidate the clinicopathological significance of overexpression of nuclear KPNA2 expression in colorectal cancers. Methods: KPNA2 expression was investigated by immunohistochemistry on tissue microarrays of 363 cases of colorectal cancer and the association of KPNA2 expression was examined with clinicopathologic features. Results: Thirty percent (30%) of colorectal cancers demonstrated overexpression of KPNA2. The overexpression of KPNA2 was significantly associated with high pN stages (p=0.005), vascular invasions (p<0.001) and lymphatic invasions (p<0.001). Multivariate Cox regression analysis showed that the overexpression of PKNA2 in pN stage 1, 2 was an independent prognostic factor of decreased survival [HR=2.13 (95% CI: 1.32-3.45, p=0.002)]. The overall survival was significantly decreased in patients of KPNA2 high expression [HR=2.70 (95% CI: 1.74-4.20, p<0.001)]. The cumulative survival was significantly decreased in patients of KPNA2 high expression compared to those of KPNA2 low expression by Kaplan-Meier analysis (log rank test, p<0.001). Conclusion: The overexpression of KPNA2 can be a valuable poor prognostic marker of colorectal cancer and the KPNA2 can be used in therapeutic strategies. Citation Format: Moo Jun Baek, Dongjun Jeong, Tae Hyun Kim, Chang-Jin Kim, Sang Han Lee, Han Jo Kim, Sang Byeong Bae, Tae Sung Ahn. Overexpression of nuclear karyopherin alpha2 correlates with poor prognosis in patients with colorectal cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2862. doi:10.1158/1538-7445.AM2014-2862