Acylglycerol kinase promotes the proliferation and cell cycle progression of oral squamous cell carcinoma

Abstract

Abstract. Cell proliferation is a major underlying cause of mortality amongst patients with oral squamous cell carcinoma (OSCC); however, the underlying mechanisms have remained to be elucidated. Acylglycerol kinase (AGK) is a multisubstrate lipid kinase, which is known to be associated with the progression of various types of human cancer. The present study aimed to investigate the role of AGK in cell proliferation and cell cycle progression in OSCC. The expression levels of AGK were detected in cancerous and adjacent normal tissue samples from four patients with OSCC undergoing surgical resection, and in OSCC cell lines, using the polymerase chain reaction (PCR) and western blot analysis. The effects of AGK on the proliferation and cell cycle progression of OSCC cells were assessed using a short hairpin RNA lentivirus or expressed-plasmid transfection. In addition, the expression levels of cyclin D1 and p21, as well as cell proliferation-and cell cycle-associated proteins were detected by PCR and western blotting. The results of the present study demonstrated that the expression levels of AGK were significantly higher in the cancerous tissues and OSCC cell lines, compared with the adjacent normal tissues and control cells, respectively. Furthermore, MTT and colony formation assays, in addition to flow cytometric analysis were conducted, in order to assess the role of AGK in cell proliferation and cell cycle progression. The cell proliferation and cell cycle progression of an established OSCC cell line were demonstrated to be decreased following AGK knockdown, and enhanced by AGK overexpression in vitro. Aberrant AGK expression in OSCC was shown to be associated with cell proliferation and cell cycle progression. The results of the present study provide evidence that AGK may promote cell proliferation and cell cycle progression in OSCC.

Acylglycerol kinase promotes tumour growth and metastasis via activating the PI3K/AKT/GSK3β signalling pathway in renal cell carcinoma

“…Therefore, further investigation of the mechanism is of great value for RCC treatment. A previous study demonstrated that AGK can regulate the cell cycle of oral squamous cell carcinoma cells [16]. Wang et al found that AGK can activate the PI3K/AKT signalling pathway and then inhibit cell cycle inhibitors in breast cancer [17].…”

“…Bektas et al confirmed that upregulation of LPA expression can increase its binding to epidermal growth factor receptor (EGFR), which changes the cytoskeletal structure, induces cell formation and promotes the metastasis of prostate cancer [10]. In addition, numerous studies have demonstrated that AGK is a powerful oncogene [11][12][13][14][15][16][17]. High expression of AGK can induce the expression of hypoxia-inducible factor 1a (HIF1a) and promote epithelial-mesenchymal transition (EMT) in cervical squamous carcinoma cells [11].…”

“…High expression of AGK is associated with poor prognosis in patients with head and neck squamous cell carcinoma [15]. AGK can regulate the cell cycle in oral squamous cell carcinoma cells [16]. Wang et al found that AGK can activate the PI3K/AKT signalling pathway and then inhibit cell cycle inhibitors in breast cancer [17].…”

Ophiopogonin D inhibits cell proliferation and induces apoptosis of human laryngocarcinoma through downregulation of cyclin�B1 and MMP‑9 and upregulation of p38‑MAPK signaling

“…Cell cycle regulation occurs mainly via two key limiting points, G1/S and G2/M (7). The main regulation factors at the G2/M phase include cyclin B, cyclin-dependent kinase 1, also termed cell division cycle (Cdc) 2, cyclin-dependent kinase 2 and Cdc25C (8).…”

Overexpression of acylglycerol kinase is associated with poorer prognosis and lymph node metastasis in nasopharyngeal carcinoma

“…By acting as a lipid kinase, AGK catalyzes the phosphorylation of acylglycerol to generate lysophosphatidic acid (LPA) [ 8 – 11 ], which is known to be involved in tumor progression [ 12 ], invasion, neovascularization, and metastasis [ 13 ]. AGK was reported to be overexpressed in prostate, breast, esophageal squamous cell carcinoma (ESCC), and oral squamous cell carcinoma [ 8 , 14 – 17 ]. Bektas et al demonstrated that overexpression of AGK enhanced the proliferation and migration of prostate cancer cells in vitro [ 8 ].…”