PTTG regulates the metabolic switch of ovarian cancer cells via the c-myc pathway
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Xiu Wang1,2, Wanxing Duan1, Xuqi Li1, Jiangbo Liu1, Donghong Li2, Lianhong Ye2, Lu Qian2, Aijun Yang2, Qinhong Xu1, Han Liu1, Qiaoshan Fu2, Erxi Wu3, Qingyong Ma1, Xin Shen4
1Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an, 710061, China
2Department of Gynecology and Obstetrics, Affiliated Guangren Hospital of Xi’an Jiaotong University, Xi’an, 710004, China
3Department of Neurosurgery, Baylor Scott & White Health, Temple, Texas, 76502, USA
4Department of Anesthesiology, First Affiliated Hospital of Medical College, Xi’an Jiaotong University, Xi’an, 710061, China
Qingyong Ma, e-mail: [email protected]
Xin Shen, e-mail: [email protected]
Keywords: human pituitary tumor-transforming gene (PTTG), metabolic switch, ovarian cancer, aerobic glycolysis, oxidative phosphorylation
Received: April 04, 2015 Accepted: October 14, 2015 Published: October 26, 2015
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.
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