TY - JOUR
T1 - PTTG regulates the metabolic switch of ovarian cancer cells via the c-myc pathway
AU - Wang, Xiu
AU - Duan, Wanxing
AU - Li, Xuqi
AU - Liu, Jiangbo
AU - Li, Donghong
AU - Ye, Lianhong
AU - Qian, Lu
AU - Yang, Aijun
AU - Xu, Qinhong
AU - Liu, Han
AU - Fu, Qiaoshan
AU - Wu, Erxi
AU - Ma, Qingyong
AU - Shen, Xin
PY - 2015
Y1 - 2015
N2 - 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.
AB - 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.
KW - Aerobic glycolysis
KW - Human pituitary tumor-transforming gene (PTTG)
KW - Metabolic switch
KW - Ovarian cancer
KW - Oxidative phosphorylation
UR - https://www.scopus.com/pages/publications/84951186742
U2 - 10.18632/oncotarget.5726
DO - 10.18632/oncotarget.5726
M3 - 文章
C2 - 26516926
AN - SCOPUS:84951186742
SN - 1949-2553
VL - 6
SP - 40959
EP - 40969
JO - Oncotarget
JF - Oncotarget
IS - 38
ER -