乳腺癌AS160分子高磷酸化与18FFDG摄取相关性研究

doi:10.3760/cma.j.issn.1673422X.2017.03.004

国际肿瘤学杂志 ›› 2017, Vol. 44 ›› Issue (3): 173-176.doi: 10.3760/cma.j.issn.1673422X.2017.03.004

乳腺癌AS160分子高磷酸化与18FFDG摄取相关性研究

卫宇,姜小华,马宁,程怡,吕桂芳,汪伟,赵金凤

200052 上海交通大学附属国际和平妇幼保健院麻醉科(卫宇)；解放军第八五医院检验病理科(姜小华、马宁、程怡、吕桂芳、汪伟、赵金凤)

出版日期:2017-03-08 发布日期:2017-02-28
通讯作者: 姜小华 E-mail:doctorjxh@126.com
基金资助:
南京军区医学科技创新课题(12Z02)

Correlation of AS160 hyperphosphorylation and 18FFDG uptaking in invasive breast cancer

Wei Yu, Jiang Xiaohua, Ma Ning, Cheng Yi, Lyu Guifang, Wang Wei, Zhao Jinfen

Department of Anesthesiology, Shanghai International Peace Maternity and Child Heath Hospital, Shanghai Jiaotong University, Shanghai 200052, China

Online:2017-03-08 Published:2017-02-28
Contact: Jiang Xiaohua E-mail:doctorjxh@126.com
Supported by:
Medical Science and Technology Innovation Project of Nanjing Military District (12Z02)

摘要/Abstract

摘要： 目的探讨乳腺癌组织中pAS160(Thr642)水平上调与肿瘤组织18F脱氧葡萄糖(FDG)摄取的关系。方法39例原发性乳腺癌患者术前行正电子发射体层显像(PET/CT)检查，记录最大摄取值(SUVmax)，采用免疫组织化学方法检测肿瘤组织中pAS160(Thr642)水平。采用Spearman检验分析pAS160与SUVmax值的相关性。结果39例原发性乳腺癌的SUVmax为6.1±2.7，与术后病理结果相对照，PET/CT检查结果有1例假阴性。pAS160(Thr642)阳性率为76.9%，乳腺癌组织SUVmax与pAS160(Thr642)阳性程度呈显著正相关(r=0.672，P＜0.001)。结论AS160在乳腺癌组织的葡萄糖代谢中起到重要的作用，其过度磷酸化可能是乳腺癌患者葡萄糖摄取的分子基础。

关键词: 乳腺肿瘤, 磷酸化, 氟脱氧葡萄糖F18, AS160

Abstract: ObjectiveTo investigate the correlation between AS160 hyperphosphorylation and 18Ffluorodeoxyglucose (18FFDG) uptaking in invasive breast cancer. MethodsThirtynine primary breast caner patients received PET/CT scan before operation and their maximum standard uptake values (SUVmax) were recorded. The levels of pAS160 (Thr642) were detected using immunohistochemical method in breast cancer tissues. The association between pAS160 (Thr642) levels and SUVmax was assessed using the Spearman nonparametric test. ResultsThe 18FFDG uptake of tumors of the 39 patients with primary breast caner was 6.1±2.7 (SUVmax). There was one false negative case in PET/CT scan imaging, compared with postoperative pathologic result. The positive rate of pAS160 (Thr642) was 76.9%, and it was positively correlated with SUVmax (r=0.672, P<0.001). ConclusionAS160 plays a significant role in the glucose metablism of breast cancer tissues and its hyperphosphorylation may contribute to the increased uptaking of glucose in patients with breast cancer.

Key words: Breast neoplasms, Phosphorylation, Fluomdeoxyglucose F18, AS160

卫宇,姜小华,马宁,程怡,吕桂芳,汪伟,赵金凤. 乳腺癌AS160分子高磷酸化与18FFDG摄取相关性研究[J]. 国际肿瘤学杂志, 2017, 44(3): 173-176.

Wei Yu, Jiang Xiaohua, Ma Ning, Cheng Yi, Lyu Guifang, Wang Wei, Zhao Jinfen. Correlation of AS160 hyperphosphorylation and 18FFDG uptaking in invasive breast cancer[J]. Journal of International Oncology, 2017, 44(3): 173-176.

参考文献

［1］ Rockall AG, Avril N, Lam R, et al. Repeatability of quantitative FDGPET/CT and contrastenhanced CT in recurrent ovarian carcinoma: testretest measurements for tumor FDG uptake, diameter, and volume［J］. Clin Cancer Res, 2014, 20(10): 2751-2760. DOI: 10.1158/10780432.CCR132634. ［2］ Geraghty KM, Chen S, Harthill JE, et al. Regulation of multisite phosphorylation and 1433 binding of AS160 in response to IGF1, EGF, PMA and AICAR［J］. Biochem J, 2007, 407(2): 231-241. DOI: 10.1042/BJ20070649. ［3］ Jiang XH, Sun JW, Xu M, et al. Frequent hyperphosphorylation of AS160 in breast cancer［J］. Cancer Biol Ther, 2010, 10(4): 362-367. ［4］ Upadhyay M, Samal J, Kandpal M, et al. The warburg effect: insights from the past decade［J］. Pharmacol Ther, 2013, 137(3): 318-330. DOI: 10.1016/j.pharmthera.2012.11.003. ［5］ Nakano I. Therapeutic potential of targeting glucose metabolism in glioma stem cells［J］. Expert Opin Ther Targets, 2014, 18(11): 1233-1236. DOI: 10.1517/14728222.2014.944899. ［6］ Reiss K, Del Valle L, Lassak A, et al. Nuclear IRS1 and cancer［J］. J Cell Physiol, 2012, 227(8): 2992-3000. DOI: 10.1002/jcp.24019. ［7］ Aleskandarany MA, Rakha EA, Ahmed MA, et al. Clinicopathologic and molecular significance of phosphoAkt expression in early invasive breast cancer［J］. Breast Cancer Res Treat, 2011, 127(2): 407-416. DOI: 10.1007/s105490101012y. ［8］ Yang S, Ji M, Zhang L, et al. Phosphorylation of KIBRA by the extracellular signalregulated kinase (ERK)ribosomal S6 kinase (RSK) cascade modulates cell proliferation and migration［J］. Cell Signal, 2014, 26(2): 343-351. DOI: 10.1016/j.cellsig.2013.11.012. ［9］ Sommer EM, Dry H, Cross D, et al. Elevated SGK1 predicts resistance of breast cancer cells to Akt inhibitors［J］. Biochem J, 2013, 452(3): 499-508. DOI: 10.1042/BJ20130342. ［10］ Szablewski L. Expression of glucose transporters in cancers［J］. Biochim Biophys Acta, 2013, 1835(2): 164-169. DOI: 10.1016/j.bbcan.2012.12.004. ［11］ Shibata K, Kajiyama H, Mizokami Y, et al. Placental leucine aminopeptidase (PLAP) and glucose transporter 4 (GLUT4) expression in benign, borderline, and malignant ovarian epithelia［J］. Gynecol Oncol, 2005, 98(1): 11-18. DOI: 10.1016/j.ygyno.2005.03.043. ［12］ Cheng JC, Mcbrayer SK, Coarfa C, et al. Expression and phosphorylation of the AS160_v2 splice variant supports GLUT4 activation and the Warburg effect in multiple myeloma［J］. Cancer Metab, 2013, 1(1): 14. DOI: 10.1186/20493002114. ［13］ Soussan M, Orlhac F, Boubaya M, et al. Relationship between tumor heterogeneity measured on FDGPET/CT and pathological prognostic factors in invasive breast cancer［J］. PLoS One, 2014, 9(4): e94017. DOI: 10.1371/journal.pone.0094017. ［14］ Gongpan P, Lu Y, Wang F, et al. AS160 controls eukaryotic cell cycle and proliferation by regulating the CDK inhibitor p21［J］. Cell Cycle, 2016, 15(13): 1733-1741. DOI: 10.1080/15384101.2016.1183853. ［15］ Mcbrayer SK, Cheng JC, Singhal S, et al. Multiple myeloma exhibits novel dependence on GLUT4, GLUT8, and GLUT11: implications for glucose transporterdirected therapy［J］. Blood, 2012, 119(20): 4686-4697. DOI: 10.1182/blood201109377846. ［16］ Zhang D, Li J, Wang F, et al. 2DeoxyDglucose targeting of glucose metabolism in cancer cells as a potential therapy［J］. Cancer Lett, 2014, 355(2): 176-183. DOI: 10.1016/j.canlet.2014.09.003.

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乳腺癌AS160分子高磷酸化与18FFDG摄取相关性研究

Correlation of AS160 hyperphosphorylation and 18FFDG uptaking in invasive breast cancer

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