| Autor: |
Chen YH; Women's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan., Wu JX; Women's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan., Yang SF; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Medical Research, Chung Shan Medical University Hospital, Taichung 40201, Taiwan., Wu YC; Department of Obstetrics and Gynecology, Changhua Christian Hospital, Changhua 50006, Taiwan., Hsiao YH; Women's Health Research Laboratory, Changhua Christian Hospital, Changhua 50006, Taiwan.; Institute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; Department of Obstetrics and Gynecology, Changhua Christian Hospital, Changhua 50006, Taiwan.; School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.; College of Medicine, Kaohsiung Medical University, Kaohsiung 807378, Taiwan.; Department of Post-Baccalaureate Medicine, College of Medicine, National Chung Hsing University, Taichung 40227, Taiwan. |
| Abstrakt: |
Cervical cancer ranks as the fourth most prevalent form of cancer and is a significant contributor to female mortality on a global scale. Pitavastatin is an anti-hyperlipidemic medication and has been demonstrated to exert anticancer and anti-inflammatory effects. Thus, the purpose of this study was to evaluate the anticancer effect of pitavastatin on cervical cancer and the underlying molecular mechanisms involved. The results showed that pitavastatin significantly inhibited cell viability by targeting cell-cycle arrest and apoptosis in Ca Ski, HeLa and C-33 A cells. Pitavastatin caused sub-G1- and G0/G1-phase arrest in Ca Ski and HeLa cells and sub-G1- and G2/M-phase arrest in C-33 A cells. Moreover, pitavastatin induced apoptosis via the activation of poly-ADP-ribose polymerase (PARP), Bax and cleaved caspase 3; inactivated the expression of Bcl-2; and increased mitochondrial membrane depolarization. Furthermore, pitavastatin induced apoptosis and slowed the migration of all three cervical cell lines, mediated by the PI3K/AKT and MAPK (JNK, p38 and ERK1/2) pathways. Pitavastatin markedly inhibited tumor growth in vivo in a cancer cell-originated xenograft mouse model. Overall, our results identified pitavastatin as an anticancer agent for cervical cancer, which might be expanded to clinical use in the future. |
