Background
Gastric cancer (GC) is a globally prevalent gastrointestinal tumor. Long non-coding RNAs (lncRNAs) are a new type of transcript which has become a hotspot of current research; however, the function of most lncRNAs in the advancement of GC is still not clear. The focus of this research was to elucidate the role and expression of lncRNA CNALPTC1 in GC.
Conclusions
Our research revealed that the CNALPTC1 promotes GC development by negatively regulating the miR-6788-5p/PAK1 pathway. GC therapy may be improved by conducting targeted studies of the CNALPTC1/miR-6788-5p/PAK1 axis.
Methods
In GC cells and tissues, the detection of CNALPTC1 expression was carried out using quantitative real-time polymerase chain reaction (qRT-PCR), and the link between its expression and clinicopathological features was investigated. The impacts of inhibition and upregulation of CNALPTC1 on the physiological behavior of GC cells were observed. Furthermore, through bioinformatics analysis and prediction of microRNA (miRNA) targeted to CNALPTC1 and target genes interacting with miRNA, the effects on invasion, proliferation, and migration of GC cells were investigated.
Results
The elevated expression level of CNALPTC1 was observed in GC tissues and cell lines. The in vitro analysis indicated that gene silencing of CNALPTC1 resulted in inhibition, whereas upregulation of CNALPTC1 resulted in the promotion of invasion, proliferation, and migration of GC cells, respectively. In addition, we observed that CNALPTC1 functions as a molecular sponge for miR-6788-5p, and the level of expression of CNALPTC1 exhibited a negative correlation with miR-6788-5p. Moreover, it was revealed that the miR-6788-5p's direct target was PAK1, which could reverse the inhibitory function of miR-6788-5p. Conclusions: Our research revealed that the CNALPTC1 promotes GC development by negatively regulating the miR-6788-5p/PAK1 pathway. GC therapy may be improved by conducting targeted studies of the CNALPTC1/miR-6788-5p/PAK1 axis.