细胞信号转导通路在甲状腺癌中的作用

doi:10.3760/cma.j.issn.1673-422X.2015.12.008

摘要/Abstract

摘要： 细胞内信号转导通路在甲状腺癌的发生和发展过程中十分重要。丝裂原活化蛋白激酶（MAPK）信号转导通路、磷脂酰肌醇3激酶（PI3K）蛋白激酶B（AKT）信号通路、核因子κB（NFκB）信号通路、RASSF1MST1FOXO3信号通路通过调节特定蛋白质的活性及表达来影响甲状腺癌的发生、发展，决定着甲状腺癌细胞的生长和凋亡。

关键词: 甲状腺肿瘤, 信号转导通路

Abstract: The intracellular signal transduction pathways play an important role in the occurrence and development of thyroid cancer. Mitogen activated protein kinase (MAPK) signal transduction pathway, phosphatidylinositol 3kinase (PI3K)AKT pathway, NFκB pathway and RASSF1MST1FOXO3 pathway affect the occurrence and development of thyroid cancer by modulating the activity and expression of specifical proteins, and determine the growth and apoptosis of thyroid cancer cells.

Key words: Thyroid neoplasms, Signal transduction pathways

徐英恺,胡洁,刘伟. 细胞信号转导通路在甲状腺癌中的作用[J]. 国际肿瘤学杂志, 2015, 42(12): 911-915.

Xu Yingkai, Hu Jie, Liu Wei. Roles of cell signaling pathways in thyroid carcinoma[J]. Journal of International Oncology, 2015, 42(12): 911-915.

参考文献

［1］ Jemal A, Bray F, Center MM, et al. Global cancer statistics［J］. CA Cancer J Clin, 2011, 61(2): 134. ［2］ Tuttle RM, Ball DW, Byrd D, et al. Thyroid carcinoma［J］. J Natl Compr Canc Netw, 2010, 8(11): 1228-1274. ［3］ Schneider DF, Chen H. New developments in the diagnosis and treatment of thyroid cancer［J］. CA Cancer J Clin, 2013, 63(6): 374-394. ［4］ Xing M. Molecular pathogenesis and mechanisms of thyroid cancer［J］. Nat Rev Cancer, 2013, 13(3): 184-199. ［5］ Omur O, Baran Y. An update on molecular biology of thyroid cancers［J］. Crit Rev Oncol Hematol, 2014, 90(3): 233-252. ［6］ Knauf JA, Fagin JA. Role of MAPK pathway oncoproteins in thyroid cancer pathogenesis and as drug targets［J］. Curr Opin Cell Biol, 2009, 21(2): 296-303. ［7］ Khan MS, Pandith AA, Azad N, et al. Impact of molecular alterations of BRAF in the pathogenesis of thyroid cancer［J］. Mutagenesis, 2014, 29(2): 131-137. ［8］ Charles RP, Silva J, Iezza G, et al. Activating BRAF and PIK3CA mutations cooperate to promote anaplastic thyroid carcinogenesis ［J］. Mol Cancer Res, 2014, 12(7): 979-986. ［9］ Watanabe R, Hayashi Y, Sassa M, et al. Possible involvement of BRAFV600E in altered gene expression in papillary thyroid cancer［J］. Endocr J, 2009, 56(3): 407-414. ［10］ Pasquali D, Santoro A, Bufo P, et al. Upregulation of endocrine glandderived vascular endothelial growth factor in papillary thyroid cancers displaying infiltrative patterns, lymph node metastases, and BRAF mutation［J］. Thyroid, 2011, 21(4): 391-399. ［11］ Zerilli M, Zito G, Martorana A, et al. BRAF(V600E) mutation influences hypoxiainducible factor 1αexpression levels in papillary thyroid cancer［J］. Mod Pathol, 2010, 23(8): 1052-1060. ［12］ Nucera C, Lawler J, Parangi S. BRAF (V600E) and thrombospondin1 promote thyroid cancer progression［J］. Cancer Res, 2011, 71(7): 2417-2422. ［13］ Knauf JA, Sartor MA, Medvedovic M, et al. Progression of BRAFinduced thyroid cancer is associated with epithelialmesenchymal transition requiring concomitant MAP kinase and TGFβ signaling［J］. Oncogene, 2011, 30(28): 3153-3162. ［14］ Khoury, Hu Q, Liu S, et al. Intarcystic papillary carcioma of breast: interrelationship with in situ and invasive carcinoma and a proposal of pathogenesis: array comparative genomic hybridization study of 14 cases［J］. Mod Pathol, 2014, 27(2): 194-203. ［15］ Tafani M, De Santis E, Coppola L, et al. Bridging hypoxia, inflammation and estrogen receptors in thyroid cancer progression［J］. Biomed Pharmacother, 2014, 68(1): 1-5. ［16］ Yamashita AS, Geraldo MV, Fuziwara CS, et al. Notch pathway is activated by MAPK signaling and influences papillary thyroid cancer prolifetration［J］. Transl Oncol, 2013, 6(2): 197-205. ［17］ ChocarroCalvo A, Zaballos MA, Santisteban P, et al. DARPP32 is required for MAPK/ERK signaling in thyroid cells［J］. Mol Endocrinol, 2012, 26(3): 471-480. ［18］ Karras S, Anagnostis P, Krassas GE. Vandetanib for the treatment of thyroid cancer: an update［J］. Expert Opin Drug Metab Toxical, 2014, 10(3): 469-481. ［19］ Gunda V, Bucur O, Varnau J, et al. Blocks to thyroid cancer cell apoptosis can be overcome by inhabitation of the MAPK and PI3K/AKT pathways［J］. Cell Death Dis, 2014, 5: e1104. ［20］ Xing M. Genetic alterations in the phosphatidylinositol 3 kinase/Akt pathway in thyroid cancer［J］. Thyroid, 2010, 20(7): 697-706. ［21］ de Biase D, Visani M, Pession A, et al. Molecular diagnosis of carcinomas of the thyroid gland［J］. Front Biosci, 2014, 6: 1-14. ［22］ Saji M, Ringel MD. The PI3K AktmTOR pathway in initiation and progression of thyroid tumors［J］. Mol Cell Endocrinol, 2010, 321(1): 20-28. ［23］ Legakis I, Syrigos K. Recent advances in molecular diagnosis of thyroid cancer［J］. J Thyroid Res, 2011, 2011: 384213. ［24］ Duman BB, Kara OI, Uˇguz A, et al. Evaluation of PTEN, PI3K, MTOR, and KRAS expression and their clinical and prognostic relevance to differentiated thyroid carcinoma［J］. Contemp Oncol (Pozn), 2014, 18(4): 234-240. ［25］ Hung CM, GarciaHaro L, Sparks CA, et al. mTORdependent cell survival mechanisms［J］. Cold Spring Harb Prespect Biol, 2012,4(12): pii a008771. ［26］ Larson SD, Silva SR, Rychahou PG, et al. PI3K/AKT activation is critical for early hepatic regeneration after partial hepatectomy［J］. Am J Physiol Gastrointest Liver Physiol, 2008, 294(6): 1401-1410. ［27］ Saji M, Narahara K, McCarty SK, et al. Akt1 deficiency delays tumor progression, vascular invasion, and distant metastasis in a murine model of thyroid cancer［J］. Oncogene, 2011, 30(42): 4307-4315. ［28］ Parke RL, Bloch A, McGuinness SP. Effect of veryhighflow nasal therapy on airway pressure and endexpiratory lung impedance in healthy volunteers［J］. Respir Care, 2015, 60(10): 1397-1403. ［29］ Pacifico F, Leonardi A. Role of NFkappaB in thyroid cancer［J］. Mol Cell Endocrinol, 2010, 321(1): 29-35. ［30］ Parker M, Mohankumar KM, Punchihewa C, et al. C11orf95RELA fusions drive oncogenic NFκB signaling in ependymomac［J］. Nature, 2014, 506(7489): 451-455. ［31］ Zhang LL, Liu J, Lei S, et al. PTEN inhibits the invasion and metastasis of gastric cancer via downregulation of FAK expression［J］. Cell Signal, 2014, 26(5): 10111020. ［32］ Li X, AbdelMageed AB, Mondal D, et al. The nuclear factor kappaB signaling pathway as a therapeutic target against thyroid cancers［J］. Thyroid, 2013, 23(2): 209-218.

[1]	王子琪, 罗盼, 叶永英, 吴伟莉. 甲状腺腺样囊性癌1例并文献复习[J]. 国际肿瘤学杂志, 2024, 51(3): 191-192.
[2]	张劲男, 刘邦卿, 李军, 刘晓辉. BHLHE40靶向HMGA2激活氧化磷酸化通路降低甲状腺癌细胞对顺铂敏感性的研究[J]. 国际肿瘤学杂志, 2023, 50(7): 398-406.
[3]	李劲浩, 王桂东, 李雪菲, 刘子琳, 孟凯龙. 静脉期CT值预测甲状腺乳头状癌中央组淋巴结转移的临床研究[J]. 国际肿瘤学杂志, 2022, 49(10): 581-585.
[4]	吴宇平, 张潇宇, 陆克义. PD-L1在甲状腺癌中的作用机制及其在诊疗中的应用[J]. 国际肿瘤学杂志, 2021, 48(9): 560-563.
[5]	冯志平, 杨传周, 陈婷, 朱家伦, 刘超, 吕娟, 陆建梅, 邓智勇. BRD4抑制剂通过BRD4/miR-106b-5p/P21分子轴特异性抑制野生型Kras分化型甲状腺癌发展[J]. 国际肿瘤学杂志, 2021, 48(8): 463-472.
[6]	侯小锋, 薛金才, 田尤新, 刘勤江. 分化型甲状腺癌诊断与外科治疗四十年[J]. 国际肿瘤学杂志, 2020, 47(8): 449-456.
[7]	程虎, 刘名奎, 陈天平. 长非编码RNA AFAP1-AS1对甲状腺癌细胞增殖和侵袭的影响及其机制[J]. 国际肿瘤学杂志, 2020, 47(6): 327-332.
[8]	王家乐, 曹君. 甲状腺癌内科治疗进展[J]. 国际肿瘤学杂志, 2020, 47(4): 231-235.
[9]	张李卓, 钱杨洋, 郑国湾, 葛明华. PD-1/PD-L1在肿瘤中的机制研究及其在甲状腺癌中的诊治价值[J]. 国际肿瘤学杂志, 2020, 47(1): 39-42.
[10]	武元元, 王军. 甲状腺未分化癌的靶向药物治疗进展[J]. 国际肿瘤学杂志, 2019, 46(2): 98-101.
[11]	董方, 薛金才, 王云生, 刘勤江. 甲状腺癌外照射放射治疗的变迁[J]. 国际肿瘤学杂志, 2019, 46(11): 641-648.
[12]	陈宏存,李良,江鸣,张军,姚宝忠,姜友,廖理芳. 甲状腺乳头状癌右侧喉返神经后方淋巴结转移的相关因素分析及其临床意义[J]. 国际肿瘤学杂志, 2018, 45(7): 391-394.
[13]	谭向荣，韩春，赵佳正，郭良. 甲状腺乳头状癌右侧喉返神经深层淋巴结转移及清扫[J]. 国际肿瘤学杂志, 2018, 45(6): 365-367.
[14]	李艳，陈琼霞，王绪明. 敲低Stat5对甲状腺癌TT细胞侵袭及上皮间质转化的影响[J]. 国际肿瘤学杂志, 2018, 45(1): 1-.
[15]	陈丽丽，蓝奎旭. 甲状腺癌的RNA相关标志物[J]. 国际肿瘤学杂志, 2017, 44(7): 534-536.