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    請使用永久網址來引用或連結此文件: http://ir.cnu.edu.tw/handle/310902800/31745

    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
    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
    顯示於類別:[醫務管理系(所)] 期刊論文


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