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.

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Nasopharyngeal carcinoma (NC) poses a threat to the life of patients. Long non-coding RNA (LncRNA) is a novel kind of non-coding RNA, which plays a pivotal role through sponge microRNA (miRNA). Abnormal expression of small nucleolar RNA host gene 8 (SNHG8) is involved in various tumors; however, the role of SNHG8 in NC remains unknown. Quantitative real-time PCR (qRT-PCR) and Western blotting was employed to detect the expression levels of SNHG8, miR-588, and high mobility group A2 (HMGA2). Cell proliferation, migration, and invasion were analyzed by CCK-8 and transwell assays. miR-588 binding sites in SNHG8 were predicted by LncBase analysis. Luciferase reporter and RNA pull-down assay were used to confirm the interaction of SNHG8 and miR-588. SNHG8 was highly expressed in NC cells. The prognosis of the patients with NC in the high expression levels of SNHG8 was poorer than that in the low expression levels. The expression of SNHG8 was closely related to tumor size, TNM stage, and distal metastasis. Knockdown of SNHG8 inhibited cell proliferation, migration, and invasion of NC. SNHG8 targeted miR-588. Inhibition of miR-588 could partially reverse the knockdown of SNHG8 in NC cells, and miR-588 targeted HMGA2. In conclusion, SNHG8 promotes proliferation, migration, and invasion of NC cells through miR-588/HMGA2 in NC as an oncogene.