TY - JOUR
T1 - Cordycepin inhibits human gestational choriocarcinoma cell growth by disrupting centrosome homeostasis
AU - Wang, Chia Yih
AU - Tsai, Shih Wei
AU - Chien, Han Hsiang
AU - Chen, Ting Yu
AU - Sheu, Shi Yuan
AU - So, Edmund Cheung
AU - Huang, Bu Miin
N1 - Funding Information:
1. We are grateful for the support from the Core Research Laboratory, College of Medicine, National Cheng Kung University.
Funding Information:
2. This study was supported by grants from An Nan Hospital, China Medical University (ANHRF108-18) to Shih-Wei Tsai.
Funding Information:
3. This study was supported by grants from the Ministry of Science and Technology (MOST106-2320-B-006-056-MY3 and MOST109-2320-B-006-042-MY3) to Chia-Yih Wang.
Funding Information:
We are grateful for the support from the Core Research Laboratory, College of Medicine, National Cheng Kung University. 2. This study was supported by grants from An Nan Hospital, China Medical University (ANHRF108-18) to Shih-Wei Tsai. 3. This study was supported by grants from the Ministry of Science and Technology (MOST106-2320-B-006-056-MY3 and MOST109-2320-B-006-042-MY3) to Chia-Yih Wang.
Publisher Copyright:
© 2020 Wang et al.
PY - 2020
Y1 - 2020
N2 - Introduction: Human gestational choriocarcinoma, a type of gestational trophoblastic disease, occurs after miscarriage, abortion, ectopic pregnancy, or molar pregnancy. Despite recent advances in the mechanism of anticancer drugs that induce human gestational choriocarcinoma apoptosis or block its growth, new therapeutic approaches are needed to be established. Cordycepin is an active anti-cancer component extracted from Cordyceps sinensis. It prevents cell proliferation both in vitro and in vivo. Materials and Methods: Here, we examined cell growth by counting cell numbers, and performing a flow cytometry assay and EdU incorporation assay. Centrosome and cytoske-leton-related structures were observed by immunofluorescence assay. The DNA damage-related signaling was examined by Western blot assay. Results: Here, we showed that cordycepin inhibited human gestational choriocarcinoma cell proliferation and induced cell death. In addition, treatment with cordycepin activated DNA-PK and ERK, thus inducing centrosome amplification and aberrant mitosis. These amplified centrosomes also disrupted microtubule arrays and actin networks, thus leading to defective cell adhesion. Furthermore, cordycepin induced autophagy for triggering cell death. Conclusion: Thus, our study demonstrates that cordycepin inhibits cell proliferation and disrupts the cytoskeleton by triggering centrosome amplification.
AB - Introduction: Human gestational choriocarcinoma, a type of gestational trophoblastic disease, occurs after miscarriage, abortion, ectopic pregnancy, or molar pregnancy. Despite recent advances in the mechanism of anticancer drugs that induce human gestational choriocarcinoma apoptosis or block its growth, new therapeutic approaches are needed to be established. Cordycepin is an active anti-cancer component extracted from Cordyceps sinensis. It prevents cell proliferation both in vitro and in vivo. Materials and Methods: Here, we examined cell growth by counting cell numbers, and performing a flow cytometry assay and EdU incorporation assay. Centrosome and cytoske-leton-related structures were observed by immunofluorescence assay. The DNA damage-related signaling was examined by Western blot assay. Results: Here, we showed that cordycepin inhibited human gestational choriocarcinoma cell proliferation and induced cell death. In addition, treatment with cordycepin activated DNA-PK and ERK, thus inducing centrosome amplification and aberrant mitosis. These amplified centrosomes also disrupted microtubule arrays and actin networks, thus leading to defective cell adhesion. Furthermore, cordycepin induced autophagy for triggering cell death. Conclusion: Thus, our study demonstrates that cordycepin inhibits cell proliferation and disrupts the cytoskeleton by triggering centrosome amplification.
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U2 - 10.2147/DDDT.S252401
DO - 10.2147/DDDT.S252401
M3 - Article
C2 - 32801639
AN - SCOPUS:85088975907
SN - 1177-8881
VL - 14
SP - 2987
EP - 3000
JO - Drug Design, Development and Therapy
JF - Drug Design, Development and Therapy
ER -