OSU-A9 inhibits pancreatic cancer cell lines by modulating p38-JAK-STAT3 signaling

doi:10.18632/oncotarget.16450

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標題:	OSU-A9 inhibits pancreatic cancer cell lines by modulating p38-JAK-STAT3 signaling
作者:	Tsai, Wan-Chi Bai, Li-Yuan Chen, Yi-Jin Chu, Po-Chen Hsu, Ya-Wen Sargeant, Aaron M. Weng, Jing-Ru
貢獻者:	Kaohsiung Med Univ, Dept Med Lab Sci & Biotechnol Kaohsiung Med Univ, Ctr Infect Dis & Canc Res China Med Univ, Coll Med China Med Univ Hosp, Div Hematol & Oncol, Dept Internal Med Acad Sinica, Inst Biol Chem Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm Charles River Labs, Safety Assessment Natl Sun Yat Sen Univ, Dept Marine Biotechnol & Resources
關鍵字:	OSU-A9 pancreatic cancer p38 JAK STAT3
日期:	2017-04-25
上傳時間:	2018-11-30 15:55:06 (UTC+8)
出版者:	Impact Journals Llc
摘要:	Pancreatic cancer is an aggressive malignancy that is the fourth leading cause of death worldwide. Since there is a dire need for novel and effective therapies to improve the poor survival rates of advanced pancreatic cancer patients, we analyzed the antitumor effects of OSU-A9, an indole-3-carbinol derivative, on pancreatic cancer cell lines in vitro and in vivo. OSU-A9 exhibited a stronger antitumor effect than gemcitabine on two pancreatic cancer cell lines, including gemcitabine-resistant PANC-1 cells. OSU-A9 treatment induced apoptosis, the down-regulation of Akt phosphorylation, up-regulation of p38 phosphorylation and decreased phosphorylation of JAK and STAT3. Cell migration and invasiveness assays showed that OSU-A9 reduced cancer cell aggressiveness and inhibited BxPC-3 xenograft growth in nude mice. These results suggest that OSU-A9 modulates the p38-JAK-STAT3 signaling module, thereby inducing cytotoxicity in pancreatic cancer cells. Continued evaluation of OSU-A9 as a potential therapeutic agent for pancreatic cancer thus appears warrented.
關聯:	Oncotarget, v.8, n.17, pp.29233-29246
显示于类别:	[醫務管理系(所)] 期刊論文

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