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// Ying-Chen Xu 1 , Chao-Jie Liang 1 , Dong-Xin Zhang 1 , Guan-Qun Li 1 , Xia Gao 1 , Jian-Zhu Fu 1 , Feng Xia 1 , Jia-Jun Ji 1 , Li-Jun Zhang 1 , Guang-Ming Li 1 and Ji-Xiang Wu 1 1 Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China Correspondence to: Ji-Xiang Wu, email: sflian2001@163.com Guang-Ming Li, email: cya_wl556@163.com Keywords: HCC, lncSHRG, SATB1, HES6, proliferation Received: March 21, 2017 Accepted: July 12, 2017 Published: August 03, 2017 ABSTRACT Hepatocellular carcinoma, one of the most common cancers, leads to mass mortality worldwide currently. However, the underlying mechanism of its oncogenesis remains to be elucidated. Here we identified that a long noncoding RNA, lncSHRG , was greatly upregulated in human hepatocellular carcinoma samples. We found that lncSHRG was essential for liver cancer cell proliferation and tumor propagation in mice. In mechanism, lncSHRG recruits SATB1 to bind to HES6 promoter and initiates HES6 expression. HES6, which is highly expressed in hepatocellular carcinoma, promotes tumor cell proliferation. High expression level of HES6 is positively correlated with clinical severity and poor prognosis of people with hepatocellular carcinoma. Altogether, our research provides a new insight on the mechanism of hepatocellular carcinoma progression.

Introduction: Choledocholithiasis is usually treated with endoscopic sphincterotomy (EST), laparoscopic common bile duct exploration (CBDE) (LCBDE), or laparoscopic transcystic CBDE (LTCBDE). However, the comparative long-term prognosis of these methods in terms of adverse outcomes remains uncertain. Methods: In an ambispective, multicenter, observational, open cohort study, patients with cholecystocholedocholithiasis underwent one of three treatments (EST+laparoscopic cholecystectomy (LC), LCBDE+LC, and LTCBDE+LC).The primary outcome was adverse outcomes. Results: At a median follow-up period of 2.72 years among 2708 patients, the adverse outcome rate is 9.3%. Compared with LCBDE and LTCBDE groups, EST group displayed an increased risk for adverse outcomes (HR 1.25, 95% CI 0.93-1.69, P=0.146; HR 1.77, 95% CI 1.30-2.43, P

Angiogenesis and JAK2 V617F mutation are common in BCR-ABL1 negative myeloproliferative neoplasms (MPNs). Ruxolitinib, a JAK inhibitor, is an effective treatment for some MPNs. However, the relationship between angiogenesis and JAK2 V617F and the effects of ruxolitinib on angiogenesis are still unknown. Here, we observed the correlation of JAK2 V617F mutation burden with VEGF, HIF-1a and microvascular density (MVD) in MPNs. We investigate the effect of ruxolitinib on the expression of VEGF and HIF-1α in JAK2 V617F positive cells. We found the expression levels of p-JAK2, VEGF, HIF-1a and MVD in the newly diagnosed MPNs were significantly increased and were related to the JAK2 V617F burden. Ruxolitinib can inhibit p-JAK2, VEGF, HIF-1a expression and suppress blood vessels’ formation in chick embryo choriallantoic membrane. Our findings indicated that angiogenesis is related to JAK2 V617F burden and ruxolitinib could decrease VEGF and HIF-1a expression in JAK2 V617F positive cells.