Elevated Sad1 and UNC84 Domain Containing 2 (SUN2) level inhibits cell growth and aerobic glycolysis in oral cancer through reducing the expressions of glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA)

Abstract Background/purpose Oral cancer is a malignant tumor accompanied by high morbidity, mortality, and poor prognosis. Therefore, it is urgent to explore the percise regulation mechanisms underlying oral cancer. Sad1 and UNC84 Domain Containing 2 (SUN2) was considered as a tumor suppressor in some cancers. The purpose of the study was to define the role of SUN2 in oral cancer progression. Materials and methods Tumor tissues and paired paracancerous healthy tissues from 56 oral cancer patients were collected. Cell viability was measured using MTT assay. The colony formation assay was applied to determine cell proliferation ability. The mRNA and protein levels were assessed by qRT-PCR and Western blot, respectively. Results SUN2 expression was decreased in oral cancer tissues and cell models. SUN2 overexpression suppressed the growth of oral cancer cells, while the down-regulation of SUN2 promoted cell growth. SUN2 overexpression restrained the glucose uptake, lactate production, and ATP level of oral cancer cells, whereas down-regulation of SUN2 promoted glycolysis. Besides, elevated SUN2 inhibited the glucose transporter 1 (GLUT1) and lactate dehydrogenase A (LDHA) levels. However, SUN2 knockdown increased the levels of GLUT1 and LDHA. Conclusion SUN2 was decreased in oral cancer in vivo and in vitro. SUN2 overexpression suppressed cell growth and glycolysis via reducing the levels of GLUT1 and LDHA in oral cancer.