BVES expression was detected in Huh7 cells transfected with Netrin-1, Netrin-1 protein was added into Huh7 cells pretreated with PI3K/Akt inhibitor LY294002 to detect the role of PI3K/Akt signaling pathway in the the change of BVES expression regulated by Netrin-1. Results: BVES was underexpressed in human HCC specimens and HCC cell lines. Huh7 cells exhibited some morphological changes including cytoskeletal rearrangement and junctional disruption after BVES inhibition. BVES inhibition promoted
migration and invasion ability. Interestingly, we found BVES expression was reduced in Huh7 cells transfected with Netrin-1, and BVES was reduced accompanyed by the increase in the phosphorylation of Akt after addition of recombinant human Netrin-1 protein. Further analysis showed that PI3K/Akt inhibitor LY294002 restored the downregulation of BVES caused by Netrin-1. Conclusion: Our study suggests that BVES can regulate Y-27632 molecular weight click here EMT of HCC cells, more importantly, we first propose
that BVES can be downregulated by Netrin-1 via PI3K/Akt signalling pathway. Key Word(s): 1. HCC; 2. EMT; 3. BVES; 4. Netrin-1; Presenting Author: YONGWEI LI Additional Authors: MINGSHENG HUANG Corresponding Author: YONGWEI LI Affiliations: The Third Affiliated Hospital of Sun Yat-sen University Objective: Tumor lysis syndrome (TLS), especially spontaneous TLS (STLS) is rare in solid cancer. Methods: We represent a patient with a large hepatocellular carcinoma (HCC). He never had a history of gouty and hyperuricemia before he had HCC. The patient showed sudden hyperuricemia up to 1026.6 μmol/L, decreased urine output and renal insufficiency, but normal potassium, phosphate, and calcium on day 49 after ineffective transcatheter artery chemoembolization (TACE). Results: Hyperuricemia was induced by tumor lysis, but it was unrelated to TACE for embolization had no direct cytotoxicity of
the chemotherapy and ischemic necrosis on the tumor, and the patient had hyperuricemia on day 49 after TACE. It was not within 3 days after effective TACE as that literatures had reported. It seemed that STLS induced hyperuricemia in the patient, while above data were not conform to the diagnostic criteria of TLS. The data showed only high risks of TLS. Aggressive hydration, Glutamate dehydrogenase oral and intravenous loop diuretic were administered, but with no allopurinol or rasburicase. The patient expired four days after onset of hyperuricemia and deterioration of liver function. Conclusion: HCC patients with high risks of TLS should be monitored intensively. Aggressive TLS prophylaxis, especially control of hyperuricemia with allopurinol or rasburicase, should be administered in patients with high risks of TLS promptly. In addition to the management of TLS, to control other concomitant symptoms is also crucial for survival. Key Word(s): 1. HCC; 2.