Abstract
Human pituitary tumor-transforming gene (PTTG) is a proto-oncogene involved in the development, invasion, and metastasis of many types of cancer, including ovarian cancer. However, little is known about the role of PTTG in the metabolic shift of ovarian cancer cells. In our study, we show that PTTG expression was positively correlated with the differentiation degree of ovarian cancer tissue. In addition, PTTG suppression by specific shRNA could inhibit the proliferation of ovarian cancer cells A2780 and SKOV-3. Furthermore, aerobic glycolysis was suppressed and oxidative phosphorylation was increased in ovarian cancer cells after PTTG suppression. We further found that the expression of c-myc and several crucial enzymes involved in aerobic glycolysis (e.g., PKM2, LDHA, and glucose transporter 1 (GLUT-1)) were downregulated by PTTG knockwown. Overexpression of c-myc could prevent the metabolic shift induced by PTTG knockwown. Together, our findings suggest that the oncogene PTTG promotes the progression of ovarian cancer cells, and its loss resists tumor development, in part, by regulating cellular metabolic reprogramming that supports cell growth and proliferation via c-myc pathway.
Highlights
Ovarian carcinoma is usually diagnosed at the advanced stage, and it has a poor prognosis that ranks fourth among the gynecological malignancies and is the most deadly gynecological cancer, with a five-year survival rate of less than 30% [1,2,3]
The results show that there was a positive correlation between pituitary tumor-transforming gene (PTTG) expression and the degree of epithelial ovarian cancer differentiation (Figure 1 and Supplementary Figure S1)
These results indicate that oncogene PTTG may promote ovarian cancer growth and development
Summary
Ovarian carcinoma is usually diagnosed at the advanced stage, and it has a poor prognosis that ranks fourth among the gynecological malignancies and is the most deadly gynecological cancer, with a five-year survival rate of less than 30% [1,2,3]. Tumor cells require much more glucose than non-cancerous cells even when there is abundant oxygen. This is in contrast to oxidative phosphorylation, which can produce more adenosine triphosphate (ATP) generated by glucose catabolism, aerobic glycolysis produces less ATP [5]. This metabolic switch can provide more intermediates for cell growth and division, and it is mainly regulated by both oncogenes and tumor suppressor gene mutants in a number of key cancerpromoting pathways [6, 7]
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