RESUMO
BACKGROUND: Accumulating evidences have been reported that long noncoding RNAs play crucial roles in the progression of hepatocellular carcinoma (HCC). SnoRNA host gene 6 (SNHG6) is believed to be involved in several human cancers, but the specific molecular mechanism of SNHG6 in HCC is not well studied. METHODS: In this study, we experimentally down-regulated the SNHG6 in two hepatocellular carcinoma cell lines in vitro, and then measured the proliferation, migration and invasion abilities and the apoptotic levels. Also, we performed the xenograft assay to investigate the function of SNHG6 during the tumor growth in vivo. RESULTS: We found SNHG6 was highly expressed in HCC tissues. Next, using Hep3B and Huh7 cells, we confirmed knockdown of SNHG6 reduced the proliferation, migration and invasion abilities in vitro. Also, by bioinformatics analysis, further molecular and cellular experiments, we found miR-6509-5p bound to SNHG6 directly, and the expression level of HIF1A was regulated through SNHG6/miR-6509-5p axis. Finally, we found that down-regulation of SNHG6 dramatically reduced the tumor growth ability of Huh7 cells in vivo. CONCLUSIONS: We concluded that SNHG6/miR-6509-5p/HIF1A axis functioned in the progression of hepatocellular carcinoma, and could be the promising therapeutic targets during the development of hepatocellular carcinoma drugs.
RESUMO
Gastric cancer (GC) is one of the serious malignant diseases, accounting for several cases globally. The prevention, discovery and cure of GC depend on its molecular mechanism. In recent decades, it has been increasingly recognized that the long noncoding RNAs (lncRNAs) have been involved in GC progression. Therefore, the present study is aimed at identifying relevant lncRNAs that could act as biomarkers for GC prognosis. LncRNA HOXA10-AS is identified to be highly expressed in GC using the ENCORI database. Kaplan-Meier plot analysis indicated that the survival rate of the patient is associated with the expression of lncRNA HOXA10-AS. Interference of HOXA10-AS inhibited GC cell proliferation, migration, and invasion as well as facilitated GC apoptosis. The targets of HOXA10-AS included miR-6509-5p and Y-box binding protein 1 (YBX1). Specifically, HOXA10-AS downregulated miR-6509-5p in GC. An increase of miR-6509-5p inhibited GC cell growth. Meanwhile, miR-6509-5p interacted with YBX1 in GC. Together, lncRNA HOXA10-AS potentially acted as an oncogene through the lncRNA HOXA10-AS/miR-6509-5p/YBX1 signaling pathway in GC.