Sumoylation in p27kip1 via RanBP2 promotes cancer cell growth in cholangiocarcinoma cell line QBC939.

Background: Cholangiocarcinoma is one of the deadly disease with poor 5-year survival and poor response to conventional therapies. Previously, we found that p27kip1 nuclear-cytoplasmic translocation confers proliferation potential to cholangiocarcinoma cell line QBC939 and this process is mediated by crm-1. However, no other post-transcriptional regulation was found in this process including sumoylation in cholangiocarcinoma.

CRM-1 knockdown inhibits extrahepatic cholangiocarcinoma tumor growth by blocking the nuclear export of p27Kip1.

Cholangiocarcinoma is a deadly disease which responds poorly to surgery and conventional chemotherapy or radiotherapy. Early diagnosis is difficult due to the anatomical and biological characteristics of cholangiocarcinoma. Cyclin-dependent kinase inhibitor 1B (p27Kip1) is a cyclin‑dependent kinase inhibitor and in the present study, we found that p27Kip1 expression was suppressed in the nucleus and increased in the cytoplasm in 53 samples of cholangiocarcinoma from patients with highly malignant tumors (poorly-differentiated and tumor-node-metastsis (TNM) stage III-IV) compared with that in samples from 10 patients with chronic cholangitis.

Immunohistochemically detected expression of Skp2, p27 kip1, and p-p27 (Thr187) in patients with cholangiocarcinoma.

The paper was aimed to detect the expression of Skp2, p27(kip1) (p27), and p-p27 (Thr187) in patients with cholangiocarcinoma (CCA). Western blot and immunohistochemistry were used to analyze the expression and subcellular localization of p27, Skp2, and p-p27 (Thr187) in tissue specimens of 53 patients with CCA and 10 with chronic proliferative cholangitis (CPC). Besides, the relationships of p27, Skp2, and p-p27 (Thr187) with clinicopathologic findings were examined, followed by analysis of the relationships of p27 expression with p-p27 (Thr187) and Skp2 in CCA tissue.