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OBJECTIVE The purpose of this study was to investigate GOLPH3 expression in nasopharyngeal carcinoma (NPC) and its influence on the metastatic ability of NPC cells; meanwhile, the underlying mechanism of GOLPH3 promoting the malignant progression of NPC was also explored. PATIENTS AND METHODS In this study, quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of GOLPH3 in 34 pairs of tumor tissue and paracancerous tissue specimens collected from NPC patients, and the interplay between GOLPH3 expression and clinical indicators was analyzed, as well as the prognosis of NPC patients. Meanwhile, GOLPH3 expression in NPC cell lines was further verified by qRT-PCR assay. Furthermore, GOLPH3 knockdown model was constructed in NPC cell lines, including SUNE2 and CNE. Then, cell counting kit-8 (CCK-8), transwell invasion, and cell wound healing assays were applied to analyze the effect of GOLPH3 on the biological function of NPC cells. In addition, an in-depth study of the relationship between GOLPH3 and E-cadherin was conducted. RESULTS QRT-PCR results indicated that the expression level of GOLPH3 in NPC was remarkably higher than that in adjacent tissues, and the difference was statistically significant. Compared with patients with low expression of GOLPH3, those with high expression of GOLPH3 had a higher incidence of lymph node metastasis. Compared with sh-NC group, the proliferation and invasive ability of NPC cells decreased remarkably after knockdown of GOLPH3. Subsequently, E-cadherin expression was found to be remarkably reduced and negatively correlated with GOLPH3 in NPC cell lines and tissues. Finally, the recovery experiment demonstrated that GOLPH3 might have a mutual regulatory relation with E-cadherin, both of which jointly affect the malignant progression of NPC. CONCLUSIONS GOLPH3 expression is remarkably associated with lymph node metastasis and poor prognosis of NPC patients; in addition, it may promote the proliferation and metastatic ability of NPC cells by regulating E-cadherin.