Gastric cancer (GC) is the fifth most common cancer in the world, with 952,000 new cases diagnosed in 2012. Tumor metastasis is the major cause of cancer recurrence and death. miR-15b-5p has been reported to be dysregulated in numerous types of cancers. However, the role of miR-15b-5p in GC metastasis remains unclear. An miRNA microarray was adopted to analyze the miRNA expression profile. By employing quantitative real-time polymerase chain reaction (qRT-PCR), miR-15b-5p expression levels were detected in GC cell lines, tissues and plasma samples. In addition, the effects of miR-15b-5p on cell proliferation, migration and invasion were studied by applying gain-of-function approaches. Moreover, the target of miR-15b-5p was assessed by dual-luciferase assay, and the mechanism underlying the regulation of GC metastasis by miR-15b-5p was assessed by rescue experiments. The results revealed that miR-15b-5p was upregulated in GC cell lines, tissues and plasma samples. A high plasma level of miR-15b-5p was correlated with distant tumor metastasis. In addition, overexpression of miR‑15b-5p in GC cells promoted cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT). Moreover, progestin and adipoQ receptor family member 3 (PAQR3) was found to be a direct target of miR-15b-5p and re-expression of PAQR3 in miR-15b-5p-overexpressing GC cells partly attenuated the proliferation, migration and invasion. These findings revealed that miR-15b-5p promotes the metastasis of GC cells through PAQR3 and may represent a potential biomarker of GC.

Purpose: MicroRNAs (miRNAs) are small endogenous, non-coding, single-stranded RNAs (approximately 22 nt). Accumulating evidence has shown that aberrant miRNA expression is pronounced and correlated with gastric cancer genesis and progression. Materials and Methods: Expression levels of miR-181a-5p in GC tissues and cell lines were assessed by qRT-PCR and tested for correlation with clinical features. In addition, effects of miR-181a-5p on GC cell growth were investigated. Results is upregulated in GC, in correlation with lymph node invasion, nerve invasion and vascular invasion (P<0.05). Enforced expression of miR-181a -5p promoted cell proliferation ability. Conclusions: This study suggested that increased miR-181a-5p is related to GC progression. MiR-181a-5p may represent a potential therapeutic target for GC.

Cinobufacin is used clinically to treat patients with many solid malignant tumors. However, the mechanisms underlying action remain to be detailed. Our study focused on miRNAs involved in cinobufacin inhibition of GC cell proliferation. miRNA microarray analysis and real time PCR identified miR-494 as a significant cinobufacinassociated miRNA. In vivo, ectopic expression of miR-494 inhibited the proliferation and induced apoptosis of BGC-823 cells on CCK-8 and flow cytometry analysis. Further study verified BAG-1 (anti-apoptosis gene) to bea target of miR-494 by luciferase reporter assay and Western blotting. In summary, our study demonstrated that cinobufacin may inhibit the proliferation and promote the apoptosis of BGC-823 cells. Cinobufacin-associated miR-494 may indirectly be involved in cell proliferation and apoptosis by targeting BAG-1, pointing to use as a potential molecular target of cinobufacin in gastric cancer therapy.

Cinobufacini is widely used in the treatment of advanced cancers. It has been previously reported that microRNA (miR)‑494 was upregulated in cinobufacini‑treated gastric cancer cells; however, the detailed role of miR‑494 in the anti‑tumor activity of cinobufacini is unclear. The present study aimed to clarify the function of miR‑494 in cinobufacini‑induced cell behavior changes. Cell viability and proliferation ability were investigated using a Cell Counting Kit‑8 assay. Flow cytometry was performed to investigate the apoptosis rate of gastric cancer (GC) cells. The mRNA expression levels of microRNA (miR)‑494 and BCL2 associated athanogene 1 (BAG‑1) were investigated using reverse transcription‑quantitative polymerase chain reaction, and the protein expression level of BAG‑1 was investigated using western blot assays. The results demonstrated that treatment with cinobufacini suppressed proliferation and promoted apoptosis of gastric cancer cells. miR‑494 acts as a tumor suppressor gene in gastric cancer. In cinobufacini‑treated cells, miR‑494 and BAG‑1 exhibited opposing expression trends. Furthermore, knockdown of miR‑494 in cinobufacini‑treated cells upregulated the protein expression level of BAG‑1, promoted cell proliferation and inhibited cell apoptosis. In addition, inhibition of BAG‑1 using small interfering RNA in cinobufacini‑treated cells partially abrogated the effects of miR‑494 inhibitor on cell proliferation and apoptosis. Thus, these results suggest that cinobufacini suppresses GC cells proliferation and promotes apoptosis partially through the regulation of miR‑494‑BAG‑1 axis, which may provide a novel insight into the functional mechanism of cinobufacini.

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Introduction: Hepatic cancer is one of the most lethal cancers and has a poor prognosis. The purpose of this study was to evaluate whether lncRNA LINC 00152 had effects on the development of hepatic cancer and the related mechanisms. Material and methods: Measuring LINC 00152 in different tissues. In in vitro experiments, we knocked down LINC 00152 expression using si-LINC00152 in HepG2 cells and evaluated cell proliferation by MTT, apoptosis by flow cytometry, invasion by Transwell, and migration by wound healing. The relative protein was evaluated by western blot. In vivo experiments included measuring tumour size and weight, using TUNEL to evaluate cell apoptosis, and measurement of relative protein expression by IHC assay. Results: In our present study, first, we found that long non-coding RNA LINC00152 expression was significantly enhanced in hepatic cancer tissues and cell lines. Second, we revealed that LINC00152 knockdown had the effect of suppressing cell proliferation and metastasis and stimulating cell apoptosis in vitro. Third, LINC00152 down-regulation significantly suppressed tumour growth and increased cell apoptosis in an in vivo experiment. Mechanistic analyses showed that LINC00152 could regulate EGFR/ PI3K/AKT/P21/MMP2/9 pathways in in vitro and in vivo experiments. Conclusions: Our results suggest that LINC00152 contributes to the oncogenic potential of hepatic cancer and that the EGFR/PI3K/AKT/P21/MMP2/9 signalling pathway might be a potential therapeutic target for hepatic cancer.