Background. Treatment options for refractory metastatic colorectal cancer (mCRC) were limited. Anlotinib is a novel multitarget tyrosine kinase inhibitor. ALTER0703 study was conducted to assess efficacy and safety of anlotinib for refractory mCRC patients.

Management of gastric cancer with malignant ascites is a challenge, and limited data are available. We evaluated factors affecting survival for this condition to determine factors that predict survival outcome and to develop a rational treatment plan. We retrospectively studied 5,542 patients with gastric adenocarcinoma from January 2007 to December 2012. Among them, 347 patients (6.26%) were associated with malignant ascites. The patients' overall survival was compared among the different features. Three hundred forty-seven patients (153 females and 194 males; median age, 53 years) were enrolled, including 78 (22.5%) young patients and 63 (18.1%) elderly patients. One hundred forty-three (41.2%) patients presented with malignant ascites at the initial diagnosis of gastric cancer, and 211 (60.8%) received chemotherapy. After a median follow-up duration of 10.4 months, the median survival after the diagnosis of malignant ascites was 5.2 months (95% CI, 4.8-5.6 months), and the 1-year survival rate was 16.1 %. An ECOG score greater than 2 (P < 0.001), the presence of ascites with the diagnosis of gastric cancer (P < 0.001), no chemotherapy (P < 0.001), an albumin level less than 30 g/L (P = 0.013), an ascites volume greater than 2,000 mL (P = 0.019), Helicobacter pylori infection (P = 0.010), and metastases to other organs (P = 0.037) were associated with poor prognosis, and they were all independent prognostic factors. The survival of gastric cancer patients with malignant ascites is relatively short, and ECOG score and the presence of ascites with the diagnosis of gastric cancer are the most important prognostic factors. Additionally, chemotherapy could improve the overall survival.

We aimed to investigate the mechanism and effects of autophagy on cisplatin (DDP)-induced apoptosis in human gastric cancer cell line SGC7901. After SGC7901 cells were treated with DDP and/or chloroquine, cell proliferation was measured using MTT assay; cell apoptosis was determined by flow cytometry; autophagy and apotosis-related proteins expression were detected by Western blot; and quantitative analysis of autophagy after monodansylcadaverine (MDC) staining was performed using fluorescence microscopy. We found after treatment with 5 mg/L DDP for 24 h, the rates of cell apoptosis were (21.07±2.12)%. Autophagy, characterized by an increase in the number of autophagic vesicles and the level of LC3-II protein was observed in cells treated with DDP. After inhibition of autophagy by chloroquine, the rates of cell apoptosis were increased to (30.16±3.54)%, and the level of Caspase-3 and P53 protein were increased, and Bcl-2 protein was decreased. Therefore, autophagy protects human gastric cancer cell line SGC7901 against DDP-induced apoptosis, inhibition of autophagy can promote apoptosis, and combination therapy with DDP and chloroquine may be a promising therapeutic strategy for gastric cancer.

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Background Numerous circular RNAs (circRNAs) are functionally investigated in various human cancers, including colorectal cancer (CRC). In this study, we explored the function of circCSNK1G1 and mechanism of action in CRC, aiming to provide evidence for circCSNK1G1 involving in CRC pathogenesis. Methods The expression of circCSNK1G1, miR-455-3p and Myosin VI (MYO6) were examined using quantitative real-time polymerase chain reaction (qRT-PCR). The functions of circCSNK1G1 on cell proliferation, apoptosis, cycle and migration/invasion were investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry assay and transwell assay, respectively. The targeted relationship between miR-455-3p and circCSNK1G1 or MYO6 predicted by bioinformatics analysis was validated using dual-luciferase reporter assay and RNA pull-down assay. The role of circCSNK1G1 was also explored in nude mice in vivo. Results The expression of circCSNK1G1 and MYO6 was elevated, while the expression of miR-455-3p was declined in CRC tissues and cells. Silencing circCSNK1G1 inhibited CRC cell proliferation, migration and invasion and induced cell apoptosis and cell cycle arrest. MiR-455-3p was a target of circCSNK1G1, and miR-455-3p could bind to MYO6. CircCSNK1G1 positively regulated MYO6 expression by targeting miR-455-3p. Inhibition of miR-455-3p reversed the effects of circCSNK1G1 silencing in CRC cells. Besides, miR-455-3p restoration blocked CRC cell growth and metastasis, which were abolished by MYO6 overexpression. Moreover, circCSNK1G1 regulated the miR-455-3p/MYO6 axis to block tumor growth in vivo. Conclusion CircCSNK1G1 participated in the progression of CRC partly by modulating the miR-455-3p/MYO6 network, which provided a theoretical basis for circCSNK1G1 involving in CRC pathogenesis, hinting that circCSNK1G1 might be a useful biomarker for CRC treatment.