PI3Kp85α在甲状腺乳头状癌中的表达及意义

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摘要目的：探讨PI3Kp85α在甲状腺乳头状癌组织中的表达及其临床意义。方法：采用免疫组织化学法、Western blot和ELISA法检测116例甲状腺乳头状癌组织、90例甲状腺乳头状增生组织中PI3Kp85α蛋白的表达情况，并分析蛋白表达与患者性别、年龄、肿瘤大小、淋巴结转移等临床病理特征的相关性。利用ROC曲线评价PI3Kp85α在甲状腺乳头状癌诊断中的价值。结果：PI3Kp85α蛋白的阳性表达率在甲状腺乳头状癌组织中显著高于甲状腺乳头状增生组织（69.8% vs. 31.1%），2组间差异有统计学意义（P＜0.05）。甲状腺乳头状癌中，PI3Kp85α蛋白表达与淋巴结转移、TNM分期相关（P＜0.05）；PI3Kp85α诊断甲状腺乳头状癌的ROC曲线下面积为0.966，当cut-off值取2.100时，诊断灵敏度（为92.2%）和特异度（为91.1%）较高。结论：甲状腺乳头状癌组织中PI3Kp85α蛋白的阳性表达率明显升高，且其表达水平与淋巴结转移和肿瘤分期相关，可能作为评估甲状腺乳头状癌侵袭性及预后的指标。

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关键词 ：甲状腺肿瘤, 磷脂酰肌醇-3激酶p85&alpha, 亚单位, 病理学, 临床, 诊断

Abstract：Objective: To explore the expression and significance of phosphatidylinositol 3-kinase regulatory subunit alpha (PI3Kp85α) in papillary thyroid carcinoma (PTC). Methods: PI3Kp85α expressions were detected in PTC tissues (n=116) and thyroid papillary hyperplasia (PTH) tissues (n=90) by immunohistochemistry, Western blot, and enzyme-linked immunosorbent assay. The relationships between PI3Kp85α expressions and clinical pathological features in PTC were analyzed. Diagnostic values of PI3Kp85α in PTC were evaluated by receiver operating characteristic (ROC) curve. Results: PI3Kp85α expression levels in PTC tissues were statistically higher than those in PTH tissues (P<0.05). PI3Kp85α expression was associated with lymph node metastasis (P<0.05). The diagnostic sensitivity and specificity of PI3Kp85α were 92.2% and 91.1%, respectively, with a cut-off value of 2.100 and an area under curve of 0.966. Conclusion: PI3Kp85α may be related to the tumorigenesis and progression of PTC.

Key words： thyroid neoplasms phosphatidylinositol 3-kinase vegulatory subunit alpha pathology, clinical diagnosis

收稿日期: 2017-11-07

基金资助:温州市科技计划项目（Y20170046）；浙江省医药卫生科技计划项目（2018KY510）。

作者简介: 龚小花（1980-），女，浙江温州人，主治医师，硕士。

链接本文:

https://xb.wmu.edu.cn/CN/ 或 https://xb.wmu.edu.cn/CN/Y2018/V48/I5/371

[1] CAMPOS M, KOOL M M J, DAMINET S, et al. Upregulation of the PI3K/Akt pathway in the tumorigenesis of canine thyroid carcinoma[J]. J Vet Intern Med, 2014, 28(6): 1814-1823.
[2] BADER A G, KANG S, ZHAO L, et al. Oncogenic PI3K deregulates transcription and translation[J]. Nat Rev Cancer, 2005, 5(12): 921-929.
[3] 张芳芳, 林秀飞, 陈聪聪, 等. Akt在FGF21预防糖尿病心肌病中的作用研究[J]. 温州医科大学学报, 2016, 46(7): 490-497.
[4] JIMÉNEZ C, HERNÁNDEZ C, PIMENTEL B, et al. The p85 regulatory subunit controls sequential activation of phosphoinositide 3-kinase by Tyr kinases and Ras[J]. J Biol Chem, 2002, 277(44): 41556-41562.
[5] YUAN T L, CANTLEY L C. PI3K pathway alterations in cancer: variations on a theme[J]. Oncogene, 2008, 27(41): 5497-5510.
[6] SOO H C, CHUNG F F L, LIM K H, et al. Cudraflavone C induces tumor-specific apoptosis in colorectal cancer cells through inhibition of the phosphoinositide 3-kinase (PI3K)-AKT pathway[J]. PLoS One, 2017, 12(1): e0170551.
[7] URICK M E, RUDD M L, GODWIN A K, et al. PIK3R1 (p85α) is somatically mutated at high frequency in primary
endometrial cancer[J]. Cancer Res, 2011, 71(12): 4061-4067.
[8] 郑永霞, 张成文, 惠斌, 等. 磷脂酰肌醇3激酶调节亚基基因对HepG2细胞增殖的影响[J]. 浙江大学学报(医学版), 2014, 43(5): 559-565.
[9] 吴迪, 刘亚林, 王梦昌. PIK3R1对多发性骨髓瘤细胞侵袭转移的影响及其机制初探[J]. 陕西医学杂志, 2015, 44(2): 134-137.
[10] 郭升超, 沈波, 赵己未, 等. PI3Kp85α对大肠癌细胞侵袭及转移的影响[J]. 广东医学, 2014, 35(4): 493-496.
[11] PETRULEA M S, PLANTINGA T S, SMIT J W, et al. PI3K/Akt/mTOR: A promising therapeutic target for non-medullary thyroid carcinoma[J]. Cancer Treat Rev, 2015, 41 (8): 707-713.
[12] DUMAN B B, KARA O I, UĞUZ A, et al. Evaluation of PTEN, PI3K MTOR, and KRAS expression and their clinical and prognostic relevance to differentiated thyroid carci-noma[J]. Contemp Oncol (Pozn), 2014, 18(4): 234-240.
[13] COSTA C, ENGELMAN J. The double life of p85[J]. Cancer Cell, 2014, 26(4): 445-447.
[14] LUO J, CANTLEY L C. The negative regulation of phosphoinositide 3-kinase signaling by p85 and it’s implication in cancer[J]. Cell Cycle, 2005, 4(10): 1309-1312.
[15] VON WILLEBRAND M, WILLIAMS S, SAXENA M, et al.
Modification of phosphatidylinositol 3-kinase SH2 domain binding properties by Abl- or Lck-mediated tyrosine phosphorylation at Tyr-688[J]. J Biol Chem, 1998, 273(7): 3994-4000.
[16] FEOLA A, CIMINI A, MIGLIUCCI F, et al. The inhibition of p85αPI3KSer83 phosphorylation prevents cell proliferation and invasion in prostate cancer cells[J]. J Biol Chem, 2013, 114(9): 2114-2119.
[17] UEKI K, FRUMAN D A, BRACHMANN S M, et al. Molecular balance between the regulatory and catalytic subunits of phosphoinositide 3-kinase regulates cell signaling and survival[J]. Mol Cell Biol, 2002, 22(3): 965-977.