博碩士論文 101224030 詳細資訊




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姓名 許博棋(Po-Chi Hsu)  查詢紙本館藏   畢業系所 生命科學系
論文名稱 綠茶表沒食子兒茶素沒食子酸酯與檳榔鹼在人類前列腺癌細胞PC-3的共同作用機制之探討
(A combinatorial study of green tea epigallocatechin gallate with arecoline on PC-3 human prostate cancer cell)
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摘要(中) 綠茶中的表沒食子兒茶素沒食子酸酯 (EGCG) 和 檳榔中的檳榔鹼 (arecoline) 都曾被報導能影響大鼠血液中的睪固酮含量和前列腺的生長,然而在人類前列腺癌細胞中卻沒有文獻去釐清 EGCG 與 arecoline 之間的交互作用。藉由雄性素非依賴型的人類前列腺癌細胞株 PC-3 ,我們發現 EGCG 對於 arecoline 減少細胞存活率的效果有協同作用。在分析生長訊息分子的過程中發現EGCG 與 arecoline混合組相較於對照組與 arecoline 單獨處理組顯著降低 cdk1 、 cdk4 和 cdk6 的表現量,但對於 cdk2 沒有顯著影響。有趣的是在觀察 cyclin 蛋白時, EGCG 會拮抗 arecoline誘導 cyclin B1 蛋白增加的效果,且 cyclin D1 和 D3 相較於單獨處理 arecoline 組,在 EGCG 混合 arecoline 組中有較低的表現量。雖然細胞週期抑制蛋白中的 p18 不受 arecoline 或 EGCG 的藥效影響,但 EGCG 卻會增強 arecoline降低 p21 蛋白表現量的效果。除此之外, EGCG 也會促進 arecoline 在自噬蛋白 LC3β-II 和凋亡蛋白 PARP 之表現量的增加效果,但 EGCG 對於 LC3β-I 則沒有影響。有趣的是, EGCG 與另一種抗氧化物 NAC 都能阻止 arecoline 所產生的 ROS ,然而 NAC 雖然能回復單獨處理 arecoline 及 EGCG 混合 arecoline組所減少的細胞存活率,但不影響單獨處理 EGCG 組所減少的細胞存活率。從以上結果推測 EGCG 和 arecoline 共同作用在 PC-3 細胞生長上的機制可能是透過調控某些路徑,如 cdk 、 cyclin 和 CKI 的家族蛋白的變化、細胞自噬和細胞凋亡的過程以及細胞中的氧化系統。
摘要(英) Green tea epigallocatechin gallate (EGCG) and betel nut arecoline have been reported to regulate blood testosterone level and prostate gland growth in rats, respectively. However, a clear interaction between EGCG and arecoline on human prostate cancer cells was not reported. Using androgen-independent human PC-3 prostate cancer cells, we found that EGCG had a synergistic effect with arecoline to reduce the cell viability. When growth signaling molecules were examined, the combination of arecoline and EGCG treatment significantly reduced the level of cylin-dependent kinase (CDK) 1, CDK4 and CDK6, but not CDK2, relative to the arecoline group or the control. Interestingly, when the endogenous CDK activators cyclins were examined, EGCG antagonized the arecoline-induced increase in cyclin B1 protein, and EGCG in combination with arecoline significantly lowered the levels of cyclins D1 and D3 compared with the arecoline group. When the endogenous CDK inhibitors (CKIs) were examined, EGCG further reduced arecoline-suppressed p21 protein level but both EGCG and arecoline had no effect on the p18 protein expression. Moreover, EGCG enhanced the arecoline-increased PARP apoptotic protein level as well as the LC3β-II but not LC3β-I autophagic protein levels. Interestingly, EGCG and the antioxidant N-acetylcysteine (NAC) were found to prevent arecoline-induced reactive oxygen species (ROS) production. However, NAC enabled to reverse the suppressive effect of arecoline, and the combination of arecoline and EGCG on cell viability, while it did not alter EGCG-induced decrease in cell viability. These results suggest that the mechanisms for the combinatorial effect of EGCG with arecoline on PC-3 cell growth may be related to certain pathways, such as the modulations of particular CDK, cyclin, and CKI family members, processes of autophagy and apoptosis, and the redox status.
關鍵字(中) ★ 前列腺癌
★ 檳榔鹼
★ 綠茶兒茶素
關鍵字(英) ★ prostate cancer
★ arecoline
★ EGCG
論文目次 中文摘要 ………………………………………………………………… i
英文摘要 ………………………………………………………………… ii
誌謝 ………………………………………………………………… iii
目錄 ………………………………………………………………… iv
縮寫對照表 ………………………………………………………………… vi
一、 前言…………………………………………………………… 1
1-1 前列腺癌……………………………………………………… 1
1-1-1 前列腺癌風險因子…………………………………………… 1
1-1-2 前列腺癌的分期……………………………………………… 1
1-1-3 前列腺癌的診斷與治療……………………………………… 2
1-1-4 氧化壓力與前列腺癌………………………………………… 2
1-2 檳榔…………………………………………………………… 3
1-2-1 檳榔子成分…………………………………………………… 3
1-2-2 檳榔生物鹼代謝……………………………………………… 3
1-2-3 檳榔生物鹼與ROS…………………………………………… 4
1-2-4 Arecoline的訊息傳遞路徑………………………………… 4
1-2-5 Arecoline與前列腺癌……………………………………… 6
1-3 茶……………………………………………………………… 6
1-3-1 茶葉的成分…………………………………………………… 6
1-3-2 兒茶素的代謝………………………………………………… 7
1-3-3 兒茶素與ROS………………………………………………… 7
1-3-4 EGCG的訊息傳遞路徑………………………………………… 8
1-3-5 EGCG與前列腺癌……………………………………………… 8
1-4 研究動機與目的……………………………………………… 9
二、 實驗材料與方法……………………………………………… 11
2-1 實驗材料……………………………………………………… 11
2-2 細胞培養……………………………………………………… 11
2-3 細胞存活率實驗……………………………………………… 11
2-4 細胞內ROS測定……………………………………………… 12
2-5 西方點墨法…………………………………………………… 12
2-5-1 12% SDS-PAGE………………………………………………… 12
2-5-2 SDS-polyacryamide 膠體電泳……………………………… 12
2-5-3 轉漬…………………………………………………………… 13
2-5-4 Blocking以及Antibody辨識……………………………… 13
2-5-5 抗體脫附……………………………………………………… 13
2-5-6 掃描與量化…………………………………………………… 14
2-6 統計分析……………………………………………………… 14
三、 結果…………………………………………………………… 15
3-1 EGCG 及 arecoline 共同抑制 PC-3 前列腺癌細胞株的細胞存活率………………………………………………………
15
3-2 EGCG 及 arecoline 影響 cdk 家族蛋白質之表現量…… 15
3-3 EGCG 及 arecoline 影響 cyclin 家族蛋白質之表現量… 16
3-4 EGCG 及 arecoline 影響 CKI 家族蛋白質之表現量…… 16
3-5 EGCG 與 arecoline 會增加細胞凋亡蛋白 PARP 之表現量………………………………………………………………
17
3-6 EGCG 及 arecoline 會增加細胞自噬蛋白 LC3β 之表現量………………………………………………………………
17
3-7 EGCG 及 arecoline 會影響細胞內 ROS 的含量………… 18
四、 討論…………………………………………………………… 19
五、 結論…………………………………………………………… 24
六、 未來與展望…………………………………………………… 25
參考文獻 ………………………………………………………………… 27
表目錄 ………………………………………………………………… 40
圖目錄 ………………………………………………………………… 46
附錄一 ………………………………………………………………… 59
參考文獻 [1] Pu, Y.-S. Prostate cancer in Taiwan: Epidemiology and risk factors. International Journal of Andrology 23, 34–36 (2000).
[2] Jian, L., Xie, L. P., Lee, A. H. & Binns, C. W. Protective effect of green tea against prostate cancer: A case-control study in southeast china. International Journal of Cancer 108, 130–135 (2003).
[3] 蒲永孝,前列腺與前列腺癌,台大醫院泌尿部、台灣楓城泌尿學會,台北,2015年。
[4] 蒲永孝,攝護腺癌治療—2016 新趨勢,台大醫院泌尿部、台灣楓城泌尿學會,台北,2016年
[5] 蒲永孝,局部性(未轉移)攝護腺癌各種治療法比較,台大醫院泌尿部、台灣楓城泌尿學會,台北,2015 年
[6] Halliwell, B. Free radicals and Antioxidants: A personal view. Nutrition Reviews 52, 253–265 (2009).
[7] Kehrer, J. P. Free radicals as mediators of tissue injury and disease. Critical Reviews in Toxicology 23, 21–48 (1993).
[8] Oberley, T. D., Zhong, W., Szweda, L. I. & Oberley, L. W. Localization of antioxidant enzymes and oxidative damage products in normal and malignant prostate epithelium. The Prostate 44, 144–155 (2000).
[9] Bostwick, D. G. et al. Human prostate cancer risk factors. Cancer 101, 2371–2490 (2004).
[10] Salisbury, R. Abstracts and reviews: ARECAIDINISM: BETEL CHEWING IN TRANSCULTURAL PERSPECTIVE by BURTON G. BURTON-BRADLEY. Canadian journal of psychiatry 24: 481-88. BETEL CHEWING DURING RECOVERY FROM PSYCHOSES: SINGLE CASE STUDY by LAWRENCE G. WILSON. Manuscript, 5 pa. Transcultural Psychiatry 17, 91–93 (1980).
[11] Nelson, B. S. & Heischober, B. Betel nut: A common drug used by naturalized citizens from India, far east Asia, and the south pacific islands. Annals of Emergency Medicine 34, 238–243 (1999).
[12] Chang, M. C. Areca nut extract and arecoline induced the cell cycle arrest but not apoptosis of cultured oral KB epithelial cells: Association of glutathione, reactive oxygen species and mitochondrial membrane potential. Carcinogenesis 22, 1527–1535 (2001).
[13] Hsing, A. W., Tsao, L. & Devesa, S. S. International trends and patterns of prostate cancer incidence and mortality. International Journal of Cancer 85, 60–67 (2000).
[14] Chang, B.-E., Liao, M.-H., Kuo, M. Y.-P. & Chen, C.-H. Developmental toxicity of arecoline, the major alkaloid in betel nuts, in zebrafish embryos. Birth Defects Research Part A: Clinical and Molecular Teratology 70, 28–36 (2004).
[15] Ko, Y.-C., Chiang, T.-A., Chang, S.-J. & Hsieh, S.-F. Prevalence of betel quid chewing habit in Taiwan and related sociodemographic factors. Journal of Oral Pathology and Medicine 21, 261–264 (1992).
[16] Cox, S., Vickers, E. R., Ghu, S. & Zoellner, H. Salivary arecoline levels during areca nut chewing in human volunteers. Journal of Oral Pathology & Medicine 39, 465–469 (2010).
[17] Nair, J. et al. Tobacco-specific and betel nut-specific N-nitroso compounds: Occurrence in saliva and urine of betel quid chewers and formation in vitro by nitrosation of betel quid. Carcinogenesis 6, 295–303 (1985).
[18] Asthana, S. et al. Clinical pharmacokinetics of arecoline in subjects with Alzheimer’s disease*. Clinical Pharmacology & Therapeutics 60, 276–282 (1996).
[19] Giri, S. et al. A Metabolomic approach to the metabolism of the Areca nut alkaloids Arecoline and Arecaidine in the mouse. Chemical Research in Toxicology 19, 818–827 (2006).
[20] Nair, U. J. et al. Formation of reactive oxygen species and of 8-hydroxydeoxyguanosine in DNA in vitro with betel quid ingredients. Chemico-Biological Interactions 63, 157–169 (1987).
[21] Chen, C.-L., Chi, C.-W. & Liu, T.-Y. HYDROXYL RADICAL FORMATION AND OXIDATIVE DNA DAMAGE INDUCED BY ARECA QUID IN VIVO. Journal of Toxicology and Environmental Health, Part A 65, 327–336 (2002).
[22] Shih, Y.-T. et al. Arecoline, a major alkaloid of the areca nut, causes neurotoxicity through enhancement of oxidative stress and suppression of the antioxidant protective system. Free Radical Biology and Medicine 49, 1471–1479 (2010).
[23] Hung, C.-R., Cheng, J.-T. & Shih, C.-S. Gastric mucosal damage induced by arecoline seizure in rats. Life Sciences 66, 2337–2349 (2000).
[24] Thangjam, G. S. & Kondaiah, P. Regulation of oxidative-stress responsive genes by arecoline in human keratinocytes. Journal of Periodontal Research 44, 673–682 (2009).
[25] Lai, K.-C. & Lee, T.-C. Genetic damage in cultured human keratinocytes stressed by long-term exposure to areca nut extracts. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 599, 66–75 (2006).
[26] Shirname, L. P., Menon, M. M., Nair, J. & Bhide, S. V. Correlation of mutagenicity and tumorigenicity of betel quid and its ingredients. Nutrition and Cancer 5, 87–91 (1983).
[27] Chang, M.-C. et al. The induction of prostaglandin E2 production, Interleukin-6 production, cell cycle arrest, and Cytotoxicity in primary oral Keratinocytes and KB cancer cells by Areca nut ingredients is Differentially regulated by MEK/ERK activation. Journal of Biological Chemistry 279, 50676–50683 (2004).
[28] Jeng, J.-H. et al. Roles of keratinocyte inflammation in oral cancer: Regulating the prostaglandin E2, interleukin-6 and TNF- production of oral epithelial cells by areca nut extract and arecoline. Carcinogenesis 24, 1301–1315 (2003).
[29] Lanzafame, A. A., Christopoulos, A. & Mitchelson, F. Cellular signaling mechanisms for Muscarinic Acetylcholine receptors. Receptors and Channels 9, 241–260 (2003).
[30] Song, P. et al. Activated Cholinergic signaling provides a target in squamous cell lung carcinoma. Cancer Research 68, 4693–4700 (2008).
[31] Song, P. et al. M3 Muscarinic receptor antagonists inhibit small cell lung carcinoma growth and Mitogen-Activated protein Kinase Phosphorylation induced by Acetylcholine secretion. Cancer Research 67, 3936–3944 (2007).
[32] An, S., Park, M.-J., Park, I.-C., Hong, S.-I. & Knox, K. Procaspase-3 and its active large subunit localized in both cytoplasm and nucleus are activated following application of apoptotic stimulus in Ramos-Burkitt lymphoma B cells. International Journal of Molecular Medicine (2003). doi:10.3892/ijmm.12.3.311
[33] 鄭靖耀,「檳榔生物鹼對於前列腺癌細胞生長和轉移的影響」,國立中央大學,碩士論文,民國102年。
[34] Chu, N.-S. Effects of betel chewing on the central and autonomic nervous systems. Journal of Biomedical Science 8, 229–236 (2001).
[35] Tillakaratne, N. J. K., Medina-Kauwe, L. & Gibson, K. M. Gamma-aminobutyric acid (GABA) metabolism in mammalian neural and nonneural tissues. Comparative Biochemistry and Physiology Part A: Physiology 112, 247–263 (1995).
[36] Chempakam, B. Hypoglycaemic activity of arecoline in betel nut Areca catechu L. Indian Journal of Experimental Biology 31, 474–475 (1993).
[37] Peungvicha, P. et al. Hypoglycemic effect of the water extract of piper sarmentosum in rats. Journal of Ethnopharmacology 60, 27–32 (1998).
[38] Sorenson, R. L., Garry, D. G. & Brelje, T. C. Structural and functional considerations of GABA in islets of Langerhans. Beta-cells and nerves. Diabetes 40, 1365–1374 (1991).
[39] Martino, G. V. et al. Autoantibodies to glutamic acid decarboxylase (GAD) detected by an immuno-trapping enzyme activity assay: Relation to insulin-dependent diabetes mellitus and islet cell antibodies. Journal of Autoimmunity 4, 915–923 (1991).
[40] Huang, L.-W. et al. Arecoline decreases interleukin-6 production and induces apoptosis and cell cycle arrest in human basal cell carcinoma cells. Toxicology and Applied Pharmacology 258, 199–207 (2012).
[41] Lee, P.-H. et al. Prolonged exposure to arecoline arrested human KB epithelial cell growth: Regulatory mechanisms of cell cycle and apoptosis. Toxicology 220, 81–89 (2006).
[42] Wang, Y.-C. et al. Arecoline arrests cells at prometaphase by deregulating mitotic spindle assembly and spindle assembly checkpoint: Implication for carcinogenesis. Oral Oncology 46, 255–262 (2010).
[43] Yang, Y.-Y. Involvement of viral and chemical factors with oral cancer in Taiwan. Japanese Journal of Clinical Oncology 34, 176–183 (2004).
[44] Saha, I., Chatterjee, A., Mondal, A., Maiti, B. R. & Chatterji, U. Arecoline augments cellular proliferation in the prostate gland of male Wistar rats. Toxicology and Applied Pharmacology 255, 160–168 (2011).
[45] Saha, I. et al. Ultrastructural and hormonal changes in the pineal–testicular axis following arecoline administration in rats. Journal of Experimental Zoology Part A: Ecological Genetics and Physiology 307A, 187–198 (2007).
[46] Shukla, Y. Tea and cancer chemoprevention: a comprehensive review. Asian Pacific journal of cancer prevention: APJCP 8, 155–166 (2007).
[47] Graham, H. N. Green tea composition, consumption, and polyphenol chemistry. Preventive Medicine 21, 334–350 (1992).
[48] Cabrera, C., Giménez, R. & López, M. C. Determination of tea components with Antioxidant activity. Journal of Agricultural and Food Chemistry 51, 4427–4435 (2003).
[49] Cabrera, C., Artacho, R. & Giménez, R. Beneficial effects of green Tea—A review. Journal of the American College of Nutrition 25, 79–99 (2006).
[50] 吳亮宜,孫璐西,科學發展,茶與健康行政院國家科學委員會,新竹,2004年。
[51] Yang, F., J.S. de Villiers, W., McClain, C. J. & Varilek, G. W. Green Tea Polyphenols Block Endotoxin-Induced Tumor Necrosis Factor-Production and Lethality in a Murine Model. Journal of Nutrition 128, 2334–2340 (1998).
[52] NAKAGAWA, K. & MIYAZAWA, T. Absorption and distribution of tea Catechin(-)-Epigallocatechin-3-Gallate, in the rat. Journal of Nutritional Science and Vitaminology, J Nutr Sci Vitaminol 43, 679–684 (1997).
[53] Chen, L., Lee, M. J., Li, H. & Yang, C. S. Absorption, distribution, elimination of tea polyphenols in rats. Drug metabolism & disposition 25, 1045–1050 (1997).
[54] Lambert, J. Cancer chemopreventive activity and bioavailability of tea and tea polyphenols. Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis 523-524, 201–208 (2003).
[55] Li, C. et al. Structural identification of Two metabolites of Catechins and their Kinetics in human urine and blood after tea ingestion. Chemical Research in Toxicology 13, 177–184 (2000).
[56] Jovanovic, S. V., Hara, Y., Steenken, S. & Simic, M. G. Antioxidant potential of Gallocatechins. A pulse Radiolysis and laser Photolysis study. Journal of the American Chemical Society 117, 9881–9888 (1995).
[57] Higdon, J. V. & Frei, B. Tea Catechins and Polyphenols: Health effects, metabolism, and Antioxidant functions. Critical Reviews in Food Science and Nutrition 43, 89–143 (2003).
[58] Rice-Evans, C. Implications of the mechanisms of action of tea Polyphenols as Antioxidants in vitro for Chemoprevention in humans. Experimental Biology and Medicine 220, 262–266 (1999).
[59] Cilliers, J. J. L. & Singleton, V. L. Nonenzymic autoxidative phenolic browning reactions in a caffeic acid model system. Journal of Agricultural and Food Chemistry 37, 890–896 (1989).
[60] VL, S. & JJL, C. Phenolic Browning-a Perspective from Grape and Wine Research. Enzymatic Browning and Its Prevention 600, 23–48 (1995).
[61] Danilewicz, J. C. Review of Reaction Mechanisms of Oxygen and Proposed Intermediate Reduction Products in Wine: Central Role of Iron and Copper. American Journal of Enology and Viticulture 54, 73–85 (2003).
[62] Wildenradt, H. L. & Singleton, V. L. Production of aldehydes as a result of oxidation of polyphenolic compounds and its relation to wine aging. American Journal of Enology and Viticulture 25, 119–126 (1974).
[63] Miller, D. Transition metals as catalysts of ‘autoxidation’ reactions. Free Radical Biology and Medicine 8, 95–108 (1990).
[64] Bandy, B. & Davison, A. J. Interactions between metals, ligands, and oxygen in the autoxidation of 6-hydroxydopamine: Mechanisms by which metal chelation enhances inhibition by superoxide dismutase. Archives of Biochemistry and Biophysics 259, 305–315 (1987).
[65] Gee, P. & Davison, A. J. 6-Hydroxydopamine does not reduce molecular oxygen directly, but requires a coreductant. Archives of Biochemistry and Biophysics 231, 164–168 (1984).
[66] Lambert, J. D. & Elias, R. J. The antioxidant and pro-oxidant activities of green tea polyphenols: A role in cancer prevention. Archives of Biochemistry and Biophysics 501, 65–72 (2010).
[67] Legeay, S., Rodier, M., Fillon, L., Faure, S. & Clere, N. Epigallocatechin Gallate: A review of its beneficial properties to prevent metabolic syndrome. Nutrients 7, 5443–5468 (2015).
[68] Lin, J.-K., Liang, Y.-C. & Lin-Shiau, S.-Y. Cancer chemoprevention by tea polyphenols through mitotic signal transduction blockade. Biochemical Pharmacology 58, 911–915 (1999).
[69] Fujimura, Y. et al. Green tea Polyphenol EGCG sensing motif on the 67-kDa Laminin receptor. PLoS ONE 7, e37942 (2012).
[70] Chen, L. & Zhang, H.-Y. Cancer preventive Mechanismsof the green tea Polyphenol (-)-Epigallocatechin-3-gallate. Molecules 12, 946–957 (2007).
[71] Nihal, M., Ahmad, N., Mukhtar, H. & Wood, G. S. Anti-proliferative and proapoptotic effects of (-)-epigallocatechin-3-gallate on human melanoma: Possible implications for the chemoprevention of melanoma. International Journal of Cancer 114, 513–521 (2005).
[72] Kavanagh, K. T. et al. Green tea extracts decrease carcinogen-induced mammary tumor burden in rats and rate of breast cancer cell proliferation in culture. Journal of Cellular Biochemistry 82, 387–398 (2001).
[73] Hastak, K. Ablation of either p21 or Bax prevents p53-dependent apoptosis induced by green tea polyphenol epigallocatechin-3-gallate. The FASEB Journal 19, 789–791 (2005).
[74] Adhami, V. M., Ahmad, N. & Mukuhtar, H. Molecular targets for green tea in prostate cancer prevention. Journal of Nutrition 133, 2417S–2424S (2003).
[75] Bhatia, N. & Agarwal, R. Detrimental effect of cancer preventive phytochemicals silymarin, genistein and epigallocatechin 3‐gallate on epigenetic events in human prostate carcinoma DU145 cells. The Prostate 46, 98–107 (2001).
[76] Casalini, P., Iorio, M. V., Galmozzi, E. & Ménard, S. Role of HER receptors family in development and differentiation. Journal of Cellular Physiology 200, 343–350 (2004).
[77] Siddiqui, I. A., Adhami, V. M., Afaq, F., Ahmad, N. & Mukhtar, H. Modulation of phosphatidylinositol-3-kinase/protein kinase B- and mitogen-activated protein kinase-pathways by tea polyphenols in human prostate cancer cells. Journal of Cellular Biochemistry 91, 232–242 (2004).
[78] Nam, S. Ester bond-containing tea Polyphenols Potently inhibit Proteasome activity in vitro and in vivo. Journal of Biological Chemistry 276, 13322–13330 (2001).
[79] 康毓琳,「以代謝體學探討檳榔鹼與綠茶對食道腫瘤的影響」,高雄醫學大學,碩士論文,民國102年。
[80] Lee, S.-S., Tsai, C.-H., Yu, C.-C. & Chang, Y.-C. Elevated snail expression Mediates tumor progression in Areca quid chewing-associated oral squamous cell carcinoma via Reactive oxygen species. PLoS ONE 8, e67985 (2013).
[81] Hsieh, Y.-P. et al. Arecoline stimulated early growth response-1 production in human buccal fibroblasts: Suppression by epigallocatechin-3-gallate. Head & Neck 37, 493–497 (2014).
[82] Ku, H.-C. et al. Green tea (-)-epigallocatechin gallate inhibits IGF-I and IGF-IIstimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor, but not aMP-activated protein kinase pathway. Molecular Nutrition & Food Research 56, 580–592 (2012).
[83] Aleem, E. & Arceci, R. J. Targeting cell cycle regulators in hematologic malignancies. Frontiers in Cell and Developmental Biology 3, (2015).
[84] Levine, B., Sinha, S. C. & Kroemer, G. Bcl-2 family members: Dual regulators of apoptosis and autophagy. Autophagy 4, 600–606 (2008).
[85] Elgendy, M., Sheridan, C., Brumatti, G. & Martin, S. J. Oncogenic Ras-Induced expression of Noxa and Beclin-1 promotes Autophagic cell death and limits Clonogenic survival. Molecular Cell 42, 23–35 (2011).
[86] Janku, F., McConkey, D. J., Hong, D. S. & Kurzrock, R. Autophagy as a target for anticancer therapy. Nature Reviews Clinical Oncology 8, 528–539 (2011).
[87] Shankar, S. Green tea polyphenols: Biology and therapeutic implications in cancer. Frontiers in Bioscience 12, 4881 (2007).
[88] Albrecht, D. S., Clubbs, E. A., Ferruzzi, M. & Bomser, J. A. Epigallocatechin-3-gallate (EGCG) inhibits PC-3 prostate cancer cell proliferation via MEK-independent ERK1/2 activation. Chemico-Biological Interactions 171, 89–95 (2008).
[89] Suganuma, M., Saha, A. & Fujiki, H. New cancer treatment strategy using combination of green tea catechins and anticancer drugs. Cancer Science 102, 317–323 (2010).
[90] Fujiki, H., Sueoka, E., Watanabe, T. & Suganuma, M. Synergistic enhancement of anticancer effects on numerous human cancer cell lines treated with the combination of EGCG, other green tea catechins, and anticancer compounds. Journal of Cancer Research and Clinical Oncology 141, 1511–1522 (2014).
[91] Fujiki, H. & Suganuma, M. Green tea: An effective synergist with anticancer drugs for tertiary cancer prevention. Cancer Letters 324, 119–125 (2012).
[92] Ji, W.-T. et al. Arecoline downregulates levels of p21 and p27 through the reactive oxygen species/mTOR complex 1 pathway and may contribute to oral squamous cell carcinoma. Cancer Science 103, 1221–1229 (2012).
[93] 楊玉燕,「口腔癌與子宮頸癌致癌因子之探討」,中山醫學院,碩士論文,民國88年。
[94] Lee, S.-S., Tsai, C.-H., Yu, C.-C. & Chang, Y.-C. Elevated snail expression Mediates tumor progression in Areca quid chewing-associated oral squamous cell carcinoma via Reactive oxygen species. PLoS ONE 8, e67985 (2013).
[95] Li, J. Cell cycle regulatory molecules (cyclins, cyclin-dependent kinases and cyclin-dependent kinase inhibitors) and the cardiovascular system; potential targets for therapy? European Heart Journal 20, 406–420 (1999).
[96] Dickinson, D. et al. Epigallocatechin-3-Gallate prevents autoimmune-associated down- regulation of p21 in salivary gland cells through a p53-Independent pathway. Inflammation & Allergy-Drug Targets 13, 15–24 (2014).
[97] Gupta, S., Hussain, T. & Mukhtar, H. Molecular pathway for (−)-epigallocatechin-3-gallate-induced cell cycle arrest and apoptosis of human prostate carcinoma cells. Archives of Biochemistry and Biophysics 410, 177–185 (2003).
[98] Singh, B. N., Shankar, S. & Srivastava, R. K. Green tea catechin, epigallocatechin-3-gallate (EGCG): Mechanisms, perspectives and clinical applications. Biochemical Pharmacology 82, 1807–1821 (2011).
[99] Zhang, X., Min, K.-W., Wimalasena, J. & Baek, S. J. Cyclin D1 degradation and p21 induction contribute to growth inhibition of colorectal cancer cells induced by epigallocatechin-3-gallate. Journal of Cancer Research and Clinical Oncology 138, 2051–2060 (2012).
[100] 吳珊瑩,「細胞自噬經由選擇性降解 cyclin D1 蛋白調控癌症發展之進程」,成功大學,博士論文,民國102年。
[101] 譚健民. 粒線體與細胞凋亡. 生物醫學 2, 250–268 (2009).
[102] Ladomery, M. Epigallocatechin-3-gallate promotes apoptosis and expression of the caspase 9a splice variant in PC3 prostate cancer cells. International Journal of Oncology (2013).
[103] Tao, L., Forester, S. C. & Lambert, J. D. The role of the mitochondrial oxidative stress in the cytotoxic effects of the green tea catechin, (-)-epigallocatechin-3-gallate, in oral cells. Molecular Nutrition & Food Research 58, 665–676 (2013).
[104] Stuart, E. C., Scandlyn, M. J. & Rosengren, R. J. Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer. Life Sciences 79, 2329–2336 (2006).
[105] Chen, S. et al. Combined cancer therapy with non-conventional drugs: All roads lead to AMPK. Mini-Reviews in Medicinal Chemistry 14, 642–654 (2014).
[106] Laio, S. The medicinal action of androgens and green tea epigallocatechin gallate. Hong Kong Medical Journal 7, 369–374 (2001).
[107] IARC. Betel-quid and areca-nut chewing and some areca-nut derived nitrosamines. IARC Monogr Eval Carcinog Risks Hum. 85, 1–334 (2004).
[108] Kao, Y.-H. Modulation of endocrine systems and food intake by green tea Epigallocatechin Gallate. Endocrinology 141, 980–987 (2000).
指導教授 高永旭(Yung-Hsi Kao) 審核日期 2016-7-19
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