Protodioscin inhibits bladder cancer cell migration and growth, and promotes apoptosis through activating JNK and p38 signaling pathways

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標題:	Protodioscin inhibits bladder cancer cell migration and growth, and promotes apoptosis through activating JNK and p38 signaling pathways
作者:	Chen, Yuan-Ru Wang, Shu-Chi Huang, Shu-Pin Su, Chia-Cheng Liu, Po-Len Cheng, Wei-Chung Chuu, Chih-Pin Chen, Jen-Kun Bao, Bo-Ying Lee, Cheng Hsueh Ke, Chien-Chih Wu, Hsin-En Chang, Hao-Han Yeh, Hsin-Chih Li, Chia-Yang
貢獻者:	Kaohsiung Medical University Kaohsiung Medical University Hospital Chi Mei Hospital Department of Senior Citizen Service Management, Chia Nan University of Pharmacy & Science China Medical University Taiwan Academia Sinica - Taiwan National Health Research Institutes - Taiwan Kaohsiung Municipal Ta-Tung Hospital
關鍵字:	methyl protodioscin dioscorea invasion injury cycle
日期:	2022
上傳時間:	2023-12-11 13:57:11 (UTC+8)
出版者:	ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
摘要:	Bladder cancer is one of the most common malignancies of the male genitourinary urinary system. Protodioscin is a steroidal saponin with anti-cancer effects on several types of cancers; however, the anti-cancer activities of protodioscin on bladder cancer have not yet been investigated. Therefore, we aimed to examine the anti-cancer effects of protodioscin on bladder cancer. Two types of bladder cancer cell lines, non-muscle-invasive 5637 cells and muscle-invasive T24 cells, were used to evaluate the effects of protodioscin on cell growth, migration, invasion and epithelial-mesenchymal transition(EMT) marker expressions. Transcriptome analysis was performed by RNA-seq and validated using real-time PCR and western blot; additionally, an in vivo xenograft animal model was established and the anti-tumor effects of protodioscin were tested. Our results demonstrated that protodioscin inhibited cell proliferation, migration, motility and invasion on 5637 and T24 cells. Additionally, protodioscin also induced cell apoptosis and arrested the progression of cell cycle at G2 phase in bladder cancer cells. Moreover, protodioscin inhibited EMT through increased protein expression of E-cadherin and decreased protein expression of N-cadherin and vimentin. RNA-seq analysis indicated that protodioscin regulated mitogenactivated protein kinase(MAPK) and phosphoinositide 3-kinases(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR) signaling pathways as further verified by Western blot. Furthermore, protodioscin
關聯:	BIOMEDICINE & PHARMACOTHERAPY, v.156, December 2022, 113929
显示于类别:	[高齡福祉養生管理系] 期刊論文

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