Up-regulated lncRNA LINC00858 facilitates proliferation and migration of gastric cancer cells.

Previous evidence has shown that the long intergenic non-protein coding RNA 858 (LINC00858) is an oncogene in non-small cell lung cancers. However, the role LINC00858 plays in gastric cancer (GC) is not clear. To illustrate the role LINC00858 plays in GC, the LINC00858 expression in GC and normal tissues was firstly detected. Then, the viability, proliferation and migration of GC BGC823 and MGC803 cells were assessed following LINC00858 knockdown by si-LINC00858 transfection. The results showed that LINC00858 had a high level of expressions in GC tissues as demonstrated by both online data and qRT-PCR assay. Also, the knockdown of LINC00858 reduced the proliferation and migration of BGC823 and MGC803 cells in vitro. Taken together, our data indicate that LINC00858 plays an oncogenic role in GC cells and might act as a potential therapeutic target for GC.

PFKFB3 Increases IL-1ß and TNF-α in Intestinal Epithelial Cells to Promote Tumorigenesis in Colitis-Associated Colorectal Cancer.

Colorectal cancer (CRC) is significantly correlated with inflammatory bowel disease, which usually manifests as chronic relapsing-remitting colitis. Phosphofructo-2-kinase/fructose-2,6-biophosphatase 3 (PFKFB3) can catalyze to produce fructose-2,6-bisphosphate and function as an oncogene. In this study, we revealed the function of PFKFB3 in colitis-associated CRC (CAC) and the potential mechanism. RT-qPCR and Western blot were utilized to detect the level of PFKFB3 expression. Increased PFKFB3 expression was observed in the mouse CAC model and CAC patient samples. We identified that overexpression of PFKFB3 in intestinal epithelial cells (IECs) could increase the proliferation, migration, and invasion of CRC cells by the coculture system. Mechanistically, overexpression of PFKFB3 induced phospho-p65 and promoted the expression of IL-1ß and tumor necrosis factor alpha (TNF-α) in the development of colitis and CAC. In addition, PFK158, the PFKFB3 inhibitor, could reduce the CRC cell viability, migration, and invasion caused by PFKFB3 overexpression. In conclusion, overexpression of PFKFB3 promoted tumorigenesis in CAC by inducing phospho-p65 and expression of IL-1ß and TNF-α. Our study suggested that PFKFB3 acted as a potential treatment target for CAC.