Background. Management of gastric cancer (GC) with liver metastases is debated. It is still controversial whether surgical resection provides a survival benefit or not. This systematic review was designed to evaluate the efficacy of hepatectomy for GC liver metastasis. Methods. We searched several electronic databases to identify eligible studies updated on September 2018. Studies assessing the efficacy and safety of hepatectomy versus no hepatectomy were included. Odds ratio (OR) along with 95% confidence interval (95% CI) were utilized for main outcome analysis. Results. In all, 10 studies were included. Patients who underwent hepatectomy had lower 1-year (OR = 0.15, 95% CI = 0.10-0.22, P < .00001), 3-year (OR = 0.16, 95% CI = 0.10-0.27, P < .00001), and 5-year mortality (OR = 0.13, 95% CI = 0.07-0.24, P < .00001) than those without hepatectomy. We also reported favorable survival outcome in patients with metachronous hepatic resection versus synchronous hepatic resection (OR = 2.09, 95% CI = 1.21-3.60, P = .008). However, there was no significant difference between solitary and multiple liver metastases (OR = 0.61, 95% CI = 0.35-1.07, P = .08). Conclusion. The present study demonstrates that hepatic resection in the management of liver metastases of GC can prolong the survival of patients and should be considered a promising treatment for such patients. Furthermore, there are more favorable outcomes in patients with metachronous metastases versus those with synchronous disease. Therefore, metachronous hepatic metastases from GC are not necessarily a contraindication for hepatectomy of the metastatic site.
Long non-coding RNAs (lncRNAs) are involved in developing hepatocellular carcinoma (HCC). The present study explored the role of lncRNA LINC01194, which is upregulated in HCC tissues and might be a vital regulator in HCC progression. Levels of LINC01194, microRNA (miR)-655-3p, and SMAD family member 5 (SMAD5) were assessed using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The bioactivity of Huh-7 cells was assessed using cell counting kit-8 and transwell assays and flow cytometry. Western blotting was conducted to measure the expression of invasion- and apoptosis-related proteins. The relationships between lncRNA LINC01194 and miR-655-3p, and miR-655-3p and SMAD5 were predicted using StarBase and TargetScan, and further verified using a dual-luciferase reporter assay. LINC01194 was overexpressed in HCC cells and in clinical samples. ILINC01194 silencing suppressed proliferation and migration; however, it promoted apoptosis in HCC cell lines. We also confirmed that miR-655-3p could bind to LINC01194, and miR-655-3p was downregulated in HCC. The upregulation of miR-655-3p suppressed HCC cell invasion and migration, and enhanced the number of apoptotic cells. SMAD5, which was overexpressed in HCC cell lines, was directly targeted by miR-655-3p. Therefore, LINC01194 promoted HCC development by decreasing miR-655-3p expression and may serve as a promising therapeutic target for HCC patients.
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