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Currently, Liver cancer is the fifth most common tumor and the second most important reason for cancer-related death in the world. However, there are still many limitations of the clinical treatment of liver cancer, and new treatment options are clearly needed. Fortunately, studies have shown that L-Selenocysteine has a certain effect on cancer. This study was to investigate the effects of L-Selenocysteine on the inhibition of cell proliferation and the promotion of apoptosis of HepG-2 cells through ROS mediated fine signaling pathway.CCK-8 assay was applied to evaluating the cytotoxic effect of L-Selenocysteine on HepG-2 cells. Electron microscopy, flow cytometry and Western Blot was utilization in further researching cells signaling pathways.The growth of HepG-2 cells was inhibited by L-selenocysteine ​​treatment in a dose-dependent manner. The cell viability decreased to 52.20%, 43.20% and 30.83% under the treatment of 4, 8, 16 µM L-selenocysteine, respectively. L-Selenocysteine had higher cytotoxicity towards HepG-2 cells than normal cells. L-Selenocysteine can induce the apoptosis of HepG-2 cells by increasing the DNA fragmentation, and activating the Caspase-3. In addition, it was found that the mechanism of the induction to HepG-2 cell apoptosis by L-Selenocysteine was closely related to the overproduction of ROS and promoted apoptosis through the Bcl-2 signaling pathway.Our data suggest that L-selenocysteine ​​may cause mitochondrial damage and subsequently stimulate ROS production. ROS can damage cellular DNA and mediate the production of Casapase-8, Bid, Bcl-2 and other proteins, affecting downstream signaling pathways, and ultimately induced apoptosis.

Objectives: Clinical and pathological significance of stage IIIC endometrial cancer is unclear. Our study was designed to determine the risk of recurrence among patients with stage IIIC endometrial cancer according to different pathological findings. Methods: We retrospectively reviewed all patients with FIGO IIIC endometrial carcinoma (n = 48) treated in our institution between 1996 and 2005. Patients without comprehensive surgical staging were excluded. Patients were classified into two groups: with adnexae and/or uterine serosal metastasis (group A, n = 18) and without metastasis (group B, n = 20). Cox proportional hazards model was used for multiple regression analysis. Results: Mean age was 64 years (range 46–90). Eighteen patients received adjuvant chemotherapy and pelvic radiotherapy, 17 received pelvic radiotherapy alone, and 11 received chemotherapy or hormonotherapy. At a median follow-up of 26.7 months, 12 had recurrence of the disease. Serosal and/or adnexal involvement was a negative independent prognostic factor for disease-free survival [relative risk = 3.75 (1.01–13.9); p = 0.04], whereas histological type, grade, depth of invasion and age at diagnosis had no influence. Conclusion: Patients with stage IIIC endometrial cancer and metastasis to adnexae and/or serosa have a higher risk of recurrence than those with node metastasis alone. Optimal adjuvant therapy for these groups remains unclear.