miR‐144‐3p facilitates nasopharyngeal carcinoma via crosstalk with PTEN

Abstract Aims This study aims to investigate the role of miR‐144‐3p and phosphatase and tensin homolog ( PTEN ) in nasopharyngeal carcinoma (NPC), along with their crosstalk with the phosphoinositide 3‐kinase (PI3K)–protein kinase B (Akt) pathway. Methods Quantitative reverse transcription polymerase chain reaction and western blot were used to measure the gene expression at the transcriptional and translational levels. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay and colony formation assay were used to examine cell proliferation via standard protocol. Transwell assay was conducted to examine cell invasiveness. A flow cytometer was used to determine cell apoptosis. Dual‐Luciferase Reporter Gene Assay (SLDL‐100) was used to confirm the target relationship between miR‐144‐3p and PTEN . Xenografts were used to detect the in vivo effects of the molecules of interest. Results miR‐144‐3p was significantly overexpressed, whereas PTEN was more underexpressed in tumor tissues than in adjacent tissues. miR‐144‐3p promoted the proliferation and invasion of NPC cells and inhibited apoptosis by directly targeting PTEN , which improves PI3K–Akt signaling. miR‐144‐3p forced epithelial–mesenchymal transition in NPC. Conclusion miR‐144‐3p promotes the progression of NPC by directly targeting PTEN via crosstalk with PI3K–Akt signaling.