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https://ir.cnu.edu.tw/handle/310902800/29741
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| 標題: | Impacts of Autophagy-Inducing Ingredient of Areca Nut on Tumor Cells |
| 作者: | Yen, Ching-Yu
Chiang, Wei-Fan
Liu, Shyun-Yeu
Lin, Chung-Chih
Liao, Kuo-An
Lin, Che-Yi
Hsieh, Wan-Fang
Cheng, Yon-Chi
Hsu, Kai-Cheng
Lin, Pin-Yen
Chen, Tai-Chi
Lee, I-Ling
Lin, Mei-Huei
Liu, Young-Chau |
| 貢獻者: | 生物科技系 |
| 關鍵字: | Activated protein-kinase
Beclin1-independent autophagy
Ampk signaling pathway
30-100 kda fraction
Cancer-cells
Cross-talk
Induction
Apoptosis
Macroautophagy
aAecoline |
| 日期: | 2015-05 |
| 上傳時間: | 2016-04-19 19:06:31 (UTC+8) |
| 出版者: | Public Library Science |
| 摘要: | Areca nut (AN) is a popular carcinogen used by about 0.6-1.2 billion people worldwide. Although AN contains apoptosis-inducing ingredients, we previously demonstrated that both AN extract (ANE) and its 30-100 kDa fraction (ANE 30-100K) predominantly induce autophagic cell death in both normal and malignant cells. In this study, we further explored the action mechanism of ANE 30-100K-induced autophagy (AIA) in Jurkat T lymphocytes and carcinoma cell lines including OECM-1 (mouth), CE81T/VGH (esophagus), SCC25 (tongue), and SCC-15 (tongue). The results showed that chemical-and small hairpin RNA (shRNA)-mediated inhibition of AMP-activated protein kinase (AMPK) resulted in the attenuation of AIA in Jurkat T but not in OECM-1 cells. Knockdown of Atg5 and Beclin 1 expressions ameliorated AIA in OECM-1/CE81T/VGH/Jurkat T and OECM-1/SCC25/SCC-15, respectively. Furthermore, ANE 30-100K could activate caspase-3 after inhibition of Beclin 1 expression in OECM-1/SCC25/SCC15 cells. Meanwhile, AMPK was demonstrated to be the upstream activator of the extracellular-regulated kinase (ERK) in Jurkat T cells, and inhibition of MEK attenuated AIA in Jurkat T/OECM-1/CE81T/VGH cells. Finally, we also found that multiple myeloma RPMI8226, lymphoma U937, and SCC15 cells survived from long-term non-cytotoxic ANE 30-100K treatment exhibited stronger resistance against serum deprivation through upregulated autophagy. Collectively, our studies indicate that Beclin-1 and Atg5 but not AMPK are commonly required for AIA, and MEK/ERK pathway is involved in AIA. Meanwhile, it is also suggested that long-term AN usage might increase the resistance of survived tumor cells against serum-limited conditions. |
| 關聯: | Plos One, v.10 n.5, Article ID e0128011 |
| 顯示於類別: | [生物科技系(所)] 期刊論文
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