Gastric cancer (GC) is a high mortality disease. We studied the function and mechanism of long non-coding RNA prostate cancer-associated transcript 6 (lncRNA PCAT6) on cell proliferation and epithelial-mesenchymal transition (EMT) in GC cells. CCK-8, flow cytometry and colony formation assay were respectively used to detect the cell viability, apoptosis and colony formation. PCAT6 and miR-15a expression were changed by cell transfection. Moreover, the level of Cyclin D1, p53, Bax, Cleaved caspase-3 and relate-proteins of EMT and cell pathways were investigated by Western blot. Besides, the level of miR-15a and PCAT6 was tested by RT-qPCR. Besides, the target relation between miR-15a and PCAT6 were tested by luciferase assay. PCAT6 was highly expressed in GC cells and tissues. Silencing of PCAT6 restrained the relate-proteins of cell proliferation and EMT. Furthermore, PCAT6 reversely regulated miR-15a and miR-15a inhibitor reversed the efficacy of sh-PCAT6 in cell proliferation and EMT. PCAT6 restrained the relate-proteins of RB/E2F and Wnt/β-catenin pathways and miR-15a reverse this progress. Finally, PCAT6 was a target of miR-15a. Silencing of lncRNA PCAT6 restrained proliferation and EMT of GC cells by targeting miR-15a via RB/E2F and Wnt/β-catenin pathways.

Gastric carcinoma (GC) is a familiar malignant carcinoma all over the world, which has high malignancy and poor prognosis. 1 Patients with early GC have a higher 5-year survival rate after surgery, but most patients are diagnosed with advanced GC at the time of admission. 2 With further research on the mechanism of GC, molecular therapy has become a hot spot in the field of GC. 3 Furthermore, a number of researches have shown that various genes are associated with GC. 4 Therefore, further research of the mechanism in GC was helpful to improve the diagnosis and treatment of GC.Circular RNAs (CircRNAs) are a type of non-coding RNAs with high tissue specificity and stable structure. 5 CircRNAs regulate the gene expression by interacting with microRNAs (miRNAs) or other molecules. 6

Gastric cancer (GC) is the third leading cause of cancer‐related death worldwide. Circular RNA circHIAT1 has been proved to play an antitumor role. We aimed to explore the function and mechanism of circHIAT1 in GC. MKN28 and MKN45 cells were transfected with PLCDH‐circHIAT1, miR‐21 mimic, and relative control. Cell viability and apoptosis were examined through Cell Counting Kit‐8 and flow cytometry, respectively. CircHIAT1 expression and other relative factors were tested through quantitative reverse transcription‐polymerase chain reaction and Western blot analysis, respectively. Our findings demonstrated that circHIAT1 was lowly expressed in GC tissues. After transfection with PLCDH‐circHIAT1 in MKN28 and MKN45 cells, cell viability was decreased, while the expression levels of p53 and p21 were raised, as well as apoptosis. Besides this, the epithelial‐mesenchymal transition process was inhibited by PLCDH‐circHIAT1 transfection. Mechanistically, miR‐21 expression was upregulated in GC tissues and could be negatively regulated by circHIAT1. Further experiments showed that the addition of miR‐21 mimic reversed the growth inhibition effects of circHIAT1 overexpression. Moreover, circHIAT1 inhibited the activation of phosphatase and tensin homolog/phosphatidylinositol 3 kinase/protein kinase B and extracellular signal‐regulated kinase signal pathways via downregulating miR‐21. CircHIAT1 functioned as a tumor inhibitor in GC cells through downregulating miR‐21, and could be a novel target for GC treatment.