Background: Nasopharyngeal carcinoma (NPC) is leading form of cancer occurring in a few well-defined regions, including southern China. NPC possess a unique and intricate etiology that remains to be elucidated. Herein, we determine expression patterns of CCNB2 and NKX3-1 and identify their roles in NPC. Materials and Methods: Gene-expression profiles of NPC in the Gene Expression Omnibus (GEO) were analyzed. Cell viability, invasion, apoptosis, cell cycle entry and mitochondrial membrane potential (MMP) were evaluated in the presence of NKX3-1 or in the absence of CCNB2. Results: In all, 187 upregulated genes and 683 downregulated genes were obtained by analyzing GSE13597. NKX3-1, the downregulated gene, and CCNB2, the upregulated one, were further confirmed by in vitro studies. Overexpression of NKX3-1 was shown to inhibit NPC cell viability and invasion. Knockdown of CCNB2 was demonstrated to reduce cell cycle entry and MMP but induce apoptosis in NPC cells. Conclusions: Taken together, the key finding obtained from the study supports CCNB2 and NKX3-1 as two promising therapeutic candidates for NPC. Molecular mechanisms that control CCNB2 or NKX3-1 disturbance require further investigation and clarification.
Background: Nasopharyngeal carcinoma (NPC) is leading form of cancer occurring in a few well-defined regions, including southern China. NPC possess a unique and intricate etiology that remains to be elucidated. Herein, we determine expression patterns of CCNB2 and NKX3-1 and identify their roles in NPC. Materials and Methods: Gene-expression profiles of NPC in the Gene Expression Omnibus (GEO) were analyzed. Cell viability, invasion, apoptosis, cell cycle entry and mitochondrial membrane potential (MMP) were evaluated in the presence of NKX3-1 or in the absence of CCNB2. Results: In all, 187 upregulated genes and 683 downregulated genes were obtained by analyzing GSE13597. NKX3-1, the downregulated gene, and CCNB2, the upregulated one, were further confirmed by in vitro studies. Overexpression of NKX3-1 was shown to inhibit NPC cell viability and invasion. Knockdown of CCNB2 was demonstrated to reduce cell cycle entry and MMP but induce apoptosis in NPC cells. Conclusions: Taken together, the key finding obtained from the study supports CCNB2 and NKX3-1 as two promising therapeutic candidates for NPC. Molecular mechanisms that control CCNB2 or NKX3-1 disturbance require further investigation and clarification.