內皮素誘導前脂肪細胞生長的訊息路徑

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蕭安淇(An-Ci Siao) 查詢紙本館藏

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生命科學系

論文名稱

內皮素誘導前脂肪細胞生長的訊息路徑
(Signal pathways of endothelins in inducing preadipocyte growth)

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摘要(中)

肥胖與糖尿病、高血壓、癌症和心血管疾病的風險有關，其特徵在於增加脂肪細胞的有絲分裂與脂肪的形成。然而，脂肪細胞的有絲分裂和脂肪形成是可以通過內分泌、遺傳、生長因子和營養來調節。本論文的總體目標主旨是在了解內皮素 (ET) 訊息途徑在控制前脂肪細胞有絲分裂作用與綠茶表沒食子兒茶素沒食子酸酯 (EGCG；主要兒茶素)、胰島素 (INS) 和類胰島素生長因子 (IGFs) 之間的關聯。這項研究的結果 (第一章) 表明第一型內皮素是透過ETAR、PKC、STAT3、AMPK、c-JUN、ERK、鞘氨醇激酶和鞘磷脂酶途徑刺激3T3-L1前脂肪細胞的生長。我們發現第三型內皮素 (第二章) 透過ETAR、AMPK、JNK/c-JUN途徑，而不是ERK與PKC途徑去刺激3T3-L1前脂肪細胞生長。這結果顯示，第一型內皮素與第三型內皮素會透過不同的訊息途徑去刺激前脂肪細胞的增生。第一型內皮素 (第三章) 可能透過ETAR、ETBR、PKC、STAT3和AMPK途徑去影響人類白色前脂肪細胞的生長。結果顯示EGCG (第四章) 透過ERK、c-Jun和SATA3途徑去抑制第一型內皮素所誘導的前脂肪細胞的生長。有趣的是我們也發現沒食子酸 (gallic acid) 與兒茶素 (catechin) 抑制第一型內皮素誘導的前脂肪細胞的生長，而表兒茶素 (epicatechin) 或表沒食子兒茶素 (epigallocatechin) 或表兒茶素沒食子酸酯 (epicatechin gallate) 則沒有這樣的作用，研究結果證明綠茶中的兒茶素具有特異性的調節作用。內皮素、胰島素或類胰島素生長因子對前脂肪細胞生長的交互作用中 (第五章)，結果表明第一型內皮素和胰島素會透過ERK途徑的協同作用來增強前脂肪細胞生長，而不是透過p38或JNK途徑。我們觀察到第二型內皮素或第三型內皮素與胰島素刺激前脂肪細胞生長具有相似的協同作用。此外，第一型內皮素、第二型內皮素、第三型內皮素都會增強類胰島素生長因子所影響的3T3-L1前脂肪細胞的生長。本文的研究結果清楚地描述各種內皮素荷爾蒙調控白色前脂肪細胞生長會透過不同的訊號途徑，並可能提供內皮素、EGCG、胰島素和類胰島素生長因子介導前脂肪細胞生長相互作用的機制，進而導致脂肪細胞活性的變化和調節脂肪細胞相關的肥胖症和其他生物醫學疾病。

摘要(英)

Obesity is associated with the risks of diabetes, hypertension, cancer, and cardiovascular diseases and is characterized with increased mitogenesis and adipogenesis of fat cells. In turn, adipocyte mitogenesis and adipogenesis can be regulated by endocrine, genetic, growth factors, and nutritional cues. The overall objective of the dissertation was designed to understand the endothelin (ET) signaling pathways in controlling preadipocyte mitogenesis in relation to green tea epigallocatechin gallate (EGCG; the major catechin), insulin (INS), and insulin-like growth factors (IGFs). The results of this study (Chapter One) indicated that ET-1 stimulated 3T3-L1 preadipocyte growth via the ETAR, PKC, STAT3, AMPK, c-JUN, ERK, sphingosine kinase, and sphingomyelinase pathways. ET-3 (Chapter Two) was found to stimulate 3T3-L1 preadipocyte growth via the ETAR, AMPK, JNK/c-JUN, but not ERK or PKC, pathways. This suggests that ET-3 exhibits somewhat different signals from ET-1 to stimulate preadipocyte proliferation. ET-1 (Chapter Three) was found to stimulate human primary preadipocyte growth possibly via the ETAR, ETBR, PKC, STAT3, and AMPK pathways. Interestingly, neither ET-2 nor ET-3 altered the growth of human white preadipocyte. EGCG (Chapter Four) was found to suppress ET-1-induced growth of 3T3-L1 preadipocytes though the ERK, c-JUN, and STAT3 pathways. Interestingly, gallic acid, catechin, but not epicatechin, or epigallocatechin, or epicatechin gallate, were also found to inhibit ET-1-induced growth of preadipocytes, suggesting the catechin-specific effect of green tea. The interactive effect of ET with INS or IGF on preadipocyte growth (Chapter Five) indicated that ET-1 and insulin had a synergistic effect on preadipocyte growth via the ERK but not p38 or JNK pathway. A similar synergistic effect of either ET-2 or ET-3 with INS to stimulate preadipocyte growth was observed. In addition, ET-1, ET-2, or ET-3 generally enhanced IGF-stimulated growth of 3T3-L1 preadipocytes. The results of this dissertation delineate distinct signal pathways of various ET hormones in controlling white preadipocyte growth and may provide a mechanism by which ETs interact with EGCG, INS, and IGF to mediate preadipocyte growth and thereby leading to changes in fat cell activity and coordinating fat cell-related obesity and other biomedical diseases.

關鍵字(中)

★ 第一型內皮素
★ 第三型內皮素
★ 胰島素
★ 類胰島素生長因子
★ 前脂肪細胞增生
★ 表沒食子兒茶素沒食子酸酯

關鍵字(英)

★ Endothelin-1
★ Endothelin-3
★ Insulin
★ insulin-like growth factors
★ Preadipocyte growth
★ Epigallocatechin gallate

論文目次

Chinese Abstract i
English Abstract ii
Declaration iv
Acknowledgments v
Table of Contents vi
List of Figures ix
List of Appendix Figures xii
Abbreviation xiii
Overall introduction 1
Chapter I – Endothelin-1 stimulates preadipocyte growth 4
I-1. Introduction 6
I-2. Materials and Methods 9
I-2.1 Chemical reagents 9
I-2.2 Cell culture 9
I-2.3 Growth stimulation experiments 10
I-2.4 Inhibitor experiments 11
I-2.5 Primary cell culture 12
I-2.6 Western blot analysis 13
I-2.7 Statistical analysis 13
I-3. Results 15
I-3.1 Effect of ET-1 on preadipocyte growth 15
I-3.2 ET-1 increases preadipocyte growth through ETAR but not ETBR 15
I-3.3 ERK and JNK are involved in the ET-1-stimulated proliferation of preadipocytes 16
I-3.4 PI3K/AKT inhibitor suppresses ET-1-induced stimulation of preadipocyte growth 18
I-3.5 JAK2/STAT3 inhibitor suppresses the ET-1 stimulation of preadipocyte growth 18
I-3.6 AMPK inhibitor suppresses the ET-1 stimulation of preadipocyte growth 19
I-3.7 PKC inhibitor suppresses the ET-1 stimulation of preadipocyte growth 20
I-3.8 SphK and SMase2 inhibitors suppress the ET-1 stimulation of preadipocyte growth 21
I-3.9 Cell type dependence of ET-1 23
I-4. Discussion 23
I-5. References 28
Chapter II – Endothelin-3 stimulates preadipocyte growth 34
II-1. Introduction 36
II-2. Materials and Methods 39
II-2.1 Chemical reagents 39
II-2.2 Cell culture 39
II-2.3 Growth stimulation experiments 39
II-2.4 Inhibitor experiments 40
II-2.5 Western blot analysis 40
II-2.6 Statistical analysis 41
II-3. Results 41
II-3.1 Effect of ET-3 on preadipocyte growth via ETAR but not ETBR 41
II-3.2 Effect of ET-3 on preadipocyte growth through ERK and JNK 42
II-3.3 Effect of ET-3 on preadipocyte growth are involved in ERK and JNK 42
II-3.4 Effect of ET-3 on preadipocyte growth via the SphK and SMase2 pathways 43
II-3.5 Cell type dependence of ET-3 44
II-4. Discussion 44
II-5. References 47
Chapter III – Endothelin-1 stimulates human preadipocyte growth 54
III-1. Introduction 56
III-2. Materials and Methods 58
III-2.1 Chemical reagents 58
III-2.2 Cell culture 58
III-2.3 Growth stimulation experiments 59
III-2.4 Western blot analysis 59
III-2.5 Statistical analysis 60
III-3. Results 61
III-3.1 ET-1 stimulated the growth of HWP-visceral cell proliferation 61
III-3.2 ET-1 increased HWP-subcutaneous cell proliferation 61
III-3.3 ET-1-stimulated HWP-visceral growth via the ETAR pathway 61
III-3.4 Different effects of various endothelin hormones in HWP-visceral cell 62
III-4. Discussion 63
III-5. References 65
Chapter IV – Green tea epigallocatechin gallate suppressed ET-1 stimulation of 3T3-L1 preadipocyte growth through the ERK, cJUN, and STAT3 pathways. 70
IV-1. Introduction 72
IV-2. Materials and Methods 74
IV-2.1 Chemical and reagents 74
IV-2.2 Cell culture 74
IV-2.3 Growth stimulation experiments 75
IV-2.4 MTT assay 76
IV-2.5 Western blot analysis 76
IV-2.6 Statistical analysis 77
IV-3. Results 78
IV-3.1 EGCG suppressed ET-1- stimulated proliferation of preadipocytes. 78
IV-3.2 EGCG suppressed ET-1-induced increase in the phosphorylation of MAPK proteins. 78
IV-3.3 EGCG suppressed ET-1-induced increase in the phosphorylation of STAT3 but not AMPK or PKC proteins. 79
IV-3.4 Other green tea catechins altered ET-1-stimulated preadipocyte growth. 79
IV-4. Discussion 81
IV-5. References 82
Chapter V - The interaction effect of endothelins with insulin and insulin-like growth factors to stimulate 3T3-L1 preadipocyte growth 92
V-1. Introduction 94
V-2. Materials and Methods 95
V-2.1 Chemical and reagents 95
V-2.2 Cell culture 95
V-2.3 Cell proliferation experiment 96
V-2.4 MTT assay 96
V-2.5 Statistical analysis 97
V-3. Results 98
V-3.1 ET-1 synergized with INS to stimulate preadipocyte growth 98
V-3.2 The ERK pathway mediated the synergistic effect of ET-1 with INS to stimulate mitogenesis of preadipocytes 98
V-3.3 ET-1 synergized with IGF to stimulate preadipocyte growth 99
V-3.4 ET-2 synergized with INS and IGF to stimulate preadipocyte growth 99
V-3.5 ET-3 synergized with INS and IGF to stimulate preadipocyte growth 100
V-4. Discussion 101
V-5. References 103
Conclusions 111
References 113

參考文獻

1. Li S, Eguchi N, Lau H, Ichii H. The Role of the Nrf2 Signaling in Obesity and Insulin Resistance. International Journal of Molecular Sciences 21: 6973, 2020.
2. Davenport AP, Hyndman KA, Dhaun N, Southan C, Kohan DE, Pollock JS, Pollock DM, Webb DJ, Maguire JJ. Endothelin. Pharmacological Reviews 68: 357–418, 2016.
3. Rubanyi GM, Polokoff MA. Endothelins: molecular biology, biochemistry, pharmacology, physiology, and pathophysiology. Pharmacological Reviews 46: 325–415, 1994.
4. Rössner S. Obesity: the disease of the twenty-first century. International Journal of Obesity 26: S2–S4, 2002.
5. Barton M, Yanagisawa M. Endothelin: 20 years from discovery to therapy. Canadian Journal of Physiology and Pharmacology 86: 485–498, 2008.
6. Nelson J, Bagnato A, Battistini B, Nisen P. The endothelin axis: emerging role in cancer. Nature Reviews Cancer 3: 110–116, 2003.
7. 59. Yanagisawa M, Kurihara H, Kimura S, Tomobe Y, Kobayashi M, Mitsui Y, Yazaki Y, Goto K, Masaki T. A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 332: 411–415, 1988.
8. Kedzierski RM, Yanagisawa M. ENDOTHELINSYSTEM: The Double-Edged Sword in Health and Disease. Annual Review of Pharmacology and Toxicology 41: 851–876, 2001.
9. Ortmann J, Nett PC, Celeiro J, Traupe T, Tornillo L, Hofmann-Lehmann R, Haas E, Frank B, Terraciano LM, Barton M. Endothelin inhibition delays onset of hyperglycemia and associated vascular injury in type I diabetes: Evidence for endothelin release by pancreatic islet β-cells. Biochemical and Biophysical Research Communications 334: 689–695, 2005.
10. Kawanabe Y, Nauli SM. Endothelin. Cellular and molecular life sciences : CMLS 68: 195–203, 2011.
11. Usui I, Imamura T, Babendure JL, Satoh H, Lu J-C, Hupfeld CJ, Olefsky JM. G protein-coupled receptor kinase 2 mediates endothelin-1-induced insulin resistance via the inhibition of both Galphaq/11 and insulin receptor substrate-1 pathways in 3T3-L1 adipocytes. Molecular Endocrinology (Baltimore, Md) 19: 2760–2768, 2005.
12. Arai H, Hori S, Aramori I, Ohkubo H, Nakanishi S. Cloning and expression of a cDNA encoding an endothelin receptor. Nature 348: 730–732, 1990.
13. Molenaar P, O’Reilly G, Sharkey A, Kuc RE, Harding DP, Plumpton C, Gresham GA, Davenport AP. Characterization and localization of endothelin receptor subtypes in the human atrioventricular conducting system and myocardium. Circulation Research 72: 526–538, 1993.
14. Idris I, Patiag D, Gray S, Donnelly R. Tissue- and time-dependent effects of endothelin-1 on insulin-stimulated glucose uptake. Biochemical Pharmacology 62: 1705–1708, 2001.
15. Barnes K, Turner AJ. The endothelin system and endothelin-converting enzyme in the brain: molecular and cellular studies. Neurochemical Research 22: 1033–1040, 1997.
16. Sakurai T, Yanagisawa M, Takuwa Y, Miyazaki H, Kimura S, Goto K, Masaki T. Cloning of a cDNA encoding a non-isopeptide-selective subtype of the endothelin receptor. Nature 348: 732–735, 1990.
17. Seo B, Oemar BS, Siebenmann R, von Segesser L, Lüscher TF. Both ETA and ETB receptors mediate contraction to endothelin-1 in human blood vessels. Circulation 89: 1203–1208, 1994.
18. Wu-Wong JR, Berg CE, Wang J, Chiou WJ, Fissel B. Endothelin stimulates glucose uptake and GLUT4 translocation via activation of endothelin ETA receptor in 3T3-L1 adipocytes. The Journal of Biological Chemistry 274: 8103–8110, 1999.
19. Lee YC, Juan CC, Fang VS, Hsu YP, Lin S-H, Kwok CF, Ho LT. Evidence that endothelin-1 (ET-1) inhibits insulin-stimulated glucose uptake in rat adipocytes mainly through ETa receptors. Metabolism 47: 1468–1471, 1998.
20. Tanahashi T, Yamaguchi K, Ishikawa S, Kusuhara M, Adachi I, Abe O. Endothelin-1 inhibits adipogenic differentiation of 3T3-L1 preadipocytes. Biochemical and Biophysical Research Communications 177: 854–860, 1991.
21. Rusznyák S, Szent-Györgyi A. Vitamin P: Flavonols as Vitamins. Nature 138: 27–27, 1936.
22. Hung PF, Wu BT, Chen HC, Chen YH, Chen CL, Wu MH, Liu HC, Lee MJ, Kao YH. Antimitogenic effect of green tea (-)-epigallocatechin gallate on 3T3-L1 preadipocytes depends on the ERK and Cdk2 pathways. American Journal of Physiology Cell Physiology 288: C1094–1108, 2005.
23. Kao YH, Chang HH, Lee MJ, Chen CL. Tea, obesity, and diabetes. Molecular Nutrition & Food Research 50: 188–210, 2006.
24. 28. Ku HC, Tsuei YW, Kao CC, Weng JT, Shih LJ, Chang HH, Liu CW, Tsai SW, Kuo YC, Kao YH. Green tea (-)-epigallocatechin gallate suppresses IGF-I and IGF-II stimulation of 3T3-L1 adipocyte glucose uptake via the glucose transporter 4, but not glucose transporter 1 pathway. General and Comparative Endocrinology 199: 46–55, 2014.
25. Kao YH, Hiipakka RA, Liao S. Modulation of obesity by a green tea catechin. The American Journal of Clinical Nutrition 72: 1232–1234, 2000.
26. Liao S, Kao YH, Hiipakka RA. Green tea: biochemical and biological basis for health benefits. Vitamins and Hormones 62: 1–94, 2001
27. Lin JK, Lin-Shiau SY. Mechanisms of hypolipidemic and anti-obesity effects of tea and tea polyphenols. Molecular Nutrition & Food Research 50: 211–217, 2006.
28. Liu HS, Chen YH, Hung PF, Kao YH. Inhibitory effect of green tea (-)-epigallocatechin gallate on resistin gene expression in 3T3-L1 adipocytes depends on the ERK pathway. American Journal of Physiology Endocrinology and Metabolism 290: E273–281, 2006.
29. Wolfram S, Wang Y, Thielecke F. Anti-obesity effects of green tea: From bedside to bench. Molecular Nutrition & Food Research 50: 176–187, 2006.
30. Wu BT, Hung PF, Chen HC, Huang RN, Chang HH, Kao YH. The apoptotic effect of green tea (-)-epigallocatechin gallate on 3T3-L1 preadipocytes depends on the Cdk2 pathway. Journal of Agricultural and Food Chemistry 53: 5695–5701, 2005.
31. 33. Lin JK, Liang YC, Lin-Shiau SY. Cancer chemoprevention by tea polyphenols through mitotic signal transduction blockade. Biochemical Pharmacology 58: 911–915, 1999.
32. Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans. The American journal of clinical nutrition 70: 1040–5, 1999.
33. Ku HC, Chang HH, Liu HC, Hsiao CH, Lee MJ, Hu YJ, Hung PF, Liu CW, Kao YH. Green tea (-)-epigallocatechin gallate inhibits insulin stimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor pathway. American Journal of Physiology Cell Physiology 297: C121–132, 2009.
34. Ku HC, Liu HS, Hung PF, Chen C-L, Liu HC, Chang HH, Tsuei YW, Shih LJ, Lin CL, Lin CM, Kao YH. Green tea (-)-epigallocatechin gallate inhibits IGF-I and IGF-II stimulation of 3T3-L1 preadipocyte mitogenesis via the 67-kDa laminin receptor, but not AMP-activated protein kinase pathway. Molecular nutrition & food research 56: 580–92, 2012.
35. Kao CC, Wu BT, Tsuei YW, Shih LJ, Kuo YL, Kao YH. Green tea catechins: inhibitors of glycerol-3-phosphate dehydrogenase. Planta Medica 76: 694–696, 2010.
36. Wang CT, Chang HH, Hsiao CH, Lee MJ, Ku HC, Hu YJ, Kao YH. The effects of green tea (-)-epigallocatechin-3-gallate on reactive oxygen species in 3T3-L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways. Molecular Nutrition & Food Research 53: 349–360, 2009.
37. Rajpathak SN, Gunter MJ, Wylie-Rosett J, Ho GYF, Kaplan RC, Muzumdar R, Rohan TE, Strickler HD. The role of insulin-like growth factor-I and its binding proteins in glucose homeostasis and type 2 diabetes. Diabetes/metabolism research and reviews 25: 3–12, 2009.
38. Kim MS, Lee DY. Insulin-like growth factor (IGF)-I and IGF binding proteins axis in diabetes mellitus. Annals of Pediatric Endocrinology & Metabolism 20: 69, 2015.
39. Froesch ER, Zapf J. Insulin-like growth factors and insulin: comparative aspects. Diabetologia 28: 485–493, 1985.
40. Baxter RC. The insulin-like growth factors and their binding proteins. Comparative Biochemistry and Physiology Part B: Comparative Biochemistry 91: 229–235, 1988.
41. LeRoith D, Werner H, Burguera B, Roberts Ct, Mulroney S, Haramati A. The insulin-like growth factor family of peptides, binding proteins and receptors: their potential role in tissue regeneration. Advances in experimental medicine and biology: 321:21-8, 1992.
42. De B, Ca G, Eo L, G J. The GH/IGF-1 axis in obesity: pathophysiology and therapeutic considerations. Nature reviews. Endocrinology 9:346-56, 2013.
43. Wilcox G. Insulin and insulin resistance. The Clinical biochemist Reviews 26: 19–39, 2005.
44. Laron Z, Werner H. Insulin: A Growth Hormone and Potential Oncogene. Pediatric endocrinology reviews: PER 17: 191–197, 2020.
45. Thevis M, Thomas A, Schänzer W. Insulin. Handbook of Experimental Pharmacology 195:209-26, 2010
46. DeLoach S, Huan Y, Daskalakis C, Falkner B. Endothelin-1 response to glucose and insulin among african americans. Journal of the American Society of Hypertension : JASH 4: 227, 2010.
47. Ferri C , Pittoni V, Piccoli A, Laurenti O , Cassone Mr , Bellini C , Properzi G, Valesini G, De Mattia G, Santucci A. Insulin stimulates endothelin-1 secretion from human endothelial cells and modulates its circulating levels in vivo. The Journal of clinical endocrinology and metabolism: 1995.
48. Sarafidis PA, Bakris GL. Insulin and Endothelin: An Interplay Contributing to Hypertension Development? The Journal of Clinical Endocrinology & Metabolism 92: 379–385, 2006.
49. Niswender KD. Basal Insulin: Physiology, Pharmacology, and Clinical Implications. Postgraduate Medicine 123: 17–26, 2011.
50. Kahn BB, Flier JS. Obesity and insulin resistance. Journal of Clinical Investigation 106: 473–481, 2000.
51. Boucher J, Softic S, El Ouaamari A, Krumpoch MT, Kleinridders A, Kulkarni RN, O’Neill BT, Kahn CR. Differential Roles of Insulin and IGF-1 Receptors in Adipose Tissue Development and Function. Diabetes 65: 2201–13, 2016.
52. Nagai M, Kamide K, Rakugi H, Takiuchi S, Imai M, Kida I, Matsukawa N, Higaki J, Ogihara T. Role of endothelin-1 induced by insulin in the regulation of vascular cell growth. American Journal of Hypertension 16: 223–228, 2003.
53. Siddle K. Signalling by insulin and IGF receptors: supporting acts and new players. Journal of molecular endocrinology 47: R1-10, 2011.
54. Clemmons DR, Maile LA. Interaction between insulin-like growth factor-I receptor and alphaVbeta3 integrin linked signaling pathways: cellular responses to changes in multiple signaling inputs. Molecular endocrinology (Baltimore, Md.)19:1-11, 2005.
55. Massoner P, Ladurner-Rennau M, Eder IE, Klocker H. Insulin-like growth factors and insulin control a multifunctional signalling network of significant importance in cancer. British Journal of Cancer 103: 1479–1484, 2010.
56. Ha WT, Jeong HY, Lee SY, Song H. Effects of the Insulin-like Growth Factor Pathway on the Regulation of Mammary Gland Development. Development & Reproduction 20: 179, 2016.
57. Hasdai D, Holmes DR, Richardson DM, Izhar U, Lerman A. Insulin and IGF-I attenuate the coronary vasoconstrictor effects of endothelin-1 but not of sarafotoxin 6c. Cardiovascular Research 39: 644–650, 1998.
58. Andronico G, Mangano M, Ferrara L, Lamanna D, Mulé G, Cerasola G. In vivo relationship between insulin and endothelin role of insulin-resistance. Journal of Human Hypertension 11: 63–66, 1997.
59. Hu RM, Levin RE, Pedram A, Frank JLH. Insulin stimulates production and secretion of endothelin from bovine endothelial cells. Diabetes 42:351-358, 1993.
60. Yuan J, Yin Z, Tao K, Wang G, Gao J. Function of insulin‑like growth factor 1 receptor in cancer resistance to chemotherapy. Oncology Letters 15:41-47, 2017

指導教授

高永旭(Yung-Hsi Kao)

審核日期

2020-11-27

推文