Chronic Stimulation of the Autophagy-inducing Ingredient of Areca Nut Promotes Tumor Growth In Vivo Through Up-regulation of Tumoral Autophagy

doi:10.21873/anticanres.13943

CNU IR > Pharmacy and Science > Dept. of Biotechnology (including master's program) > Periodical Articles > Item 310902800/34104

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题名:	Chronic Stimulation of the Autophagy-inducing Ingredient of Areca Nut Promotes Tumor Growth In Vivo Through Up-regulation of Tumoral Autophagy
作者:	Chiu, Chang-Ta Liu, Shyun-Yeu Yen, Ching-Yu Liu, Bang-Yen Sun, Zi-Yu Wu, Chun-Yi Deng, Ji-Lung Liu, Young-Chau Lin, Mei-Huei
贡献者:	China Med Univ, An Nan Hosp, Dept Dent Chi Mei Med Ctr, Oral & Maxillofacial Surg Sect Taipei Med Univ, Dept Dent Natl Def Med Ctr, Dept Dent Chia Nan Univ Pharm, Dept Biotechnol Chi Mei Med Ctr, Dept Med Res Shu Te Univ, Div Nat Sci, Coll Liberal Educ
关键词:	Areca nut autophagy nude mice 3-methyladenine chloroquine cisplatin
日期:	2020
上传时间:	2022-11-18 11:24:06 (UTC+8)
出版者:	Int Inst Anticancer Research
摘要:	Background/aim: Autophagy can be either tumor promotive or suppressive. We previously identified an autophagy-inducing activity in the 30-100 kDa fraction of areca-nut-extract (ANE 30-100K) and showed that several tumor cells subjected to chronic ANE 30-100K stimulation (CAS) exhibited higher resistance against stressed environments including serum-free (SF) conditions in vitro. Herein, we aimed to assess whether CAS can also provide growth advantages for tumor cells in vivo and the therapeutic effect of autophagy inhibition on CAS-treated tumors. Materials and Methods: Esophageal CE81T/VGH cells and nude mice were used as experimental models. Autophagy inhibitors 3-methyladenine (3-MA) and chloroquine (CQ), as well as another anticancer drug cisplatin (DDP), were chosen to challenge CAS-treated CE81T/VGH cells in vitro and in vivo. Results: CAS-treated CE81T/VGH cells expressed higher levels of microtubuleassociated protein 1 light chain 3A/B-II (LC3-II) and beclin 1 proteins, and showed stronger resistance to SF and hypoxia conditions, that were mitigated by CQ or 3-MA in vitro. Furthermore, CAS-treated CE81T/VGH cells induced significantly larger tumors in mice, which were also attenuated by single 3-MA or CQ treatment. Finally, the combined treatment of 3-MA or CQ with DDP further upregulated DDP-induced caspase-3 activity in vitro and exhibited synergistic anti-tumor effects on mice. Conclusion: CAS may up-regulate tumoral autophagy and provide growth advantage for tumors both in vitro and in vivo. Furthermore, autophagy inhibition alone or in combination with DDP may achieve positive therapy for tumors encountered with CAS.
關聯:	Anticancer Research, v.40, n.1, pp.7
显示于类别:	[Dept. of Biotechnology (including master's program)] Periodical Articles

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