期刊
ONCOTARGET
卷 8, 期 17, 页码 29233-29246出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16450
关键词
OSU-A9; pancreatic cancer; p38; JAK; STAT3
资金
- National Science Council [NSC 101-2320-B-039-029MY2]
- Ministry of Science and Technology [MOST 103-2320-B-110-006-MY3]
- National Sun Yat-Sen University-Kaoshiung Medical University Joint Research Project [NSYSU-KMU 105-I008]
- Kaohsiung Medical University [KMU-TP104E29]
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.
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