Long non-coding RNA PICART1 inhibits cell proliferation by regulating the PI3K/AKT and MAPK/ERK signaling pathways in gastric cancer.

OBJECTIVE

Gastric cancer (GC) is one of the most frequent malignancies and the second leading cause of cancer-related death in the world. The aim of this work was to illustrate the functional role of long non-coding RNA (lnRNA)-PICART1 (p53-inducible cancer-associated RNA transcript 1) in GC, thereby providing novel insights into biomarkers and therapeutic strategies in GC.

PATIENTS AND METHODS

The relative expression level of lncRNA-PICART1 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay and colony formation assay were used to determine the ability of cell proliferation. Flow cytometric analysis was performed to detect cell cycle and cell apoptosis. The protein expressions of ERK, p-ERK, AKT and p-AKT were detected by Western blotting. Furthermore, the transfected cells were used to perform tumor xenograft formation assay.

RESULTS

LncRNA-PICART1 was lowly expressed in both GC tissues and cell lines. CCK-8 assay, colony formation assay and flow cytometric analysis validated that up-regulated lncRNA-PICART1 significantly suppressed cell proliferation, whereas promoted cell apoptosis. Besides, the over-expression of lncRNA-PICART1 remarkably inhibited the PI3K/AKT and ERK/MAPK signaling pathways. Tumor xenograft formation assay indicated that lncRNA-PICART1 overexpression significantly inhibited tumor formation.

CONCLUSIONS

Our research illustrated that lncRNA-PICART1 functioned as a tumor suppressor in GC. The regulation of the PI3K/AKT and ERK/MAPK signaling pathways might be the underlying mechanism of the tumor suppressor role of lncRNA-PICART1. In addition, our study might bring novel insights into biomarkers and therapeutic strategies for GC.