MMRN2在乳腺癌中的表达及对预后的影响

摘要
图/表
参考文献(20)
相关文章 (15)

全文: PDF (769 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要目的研究多聚蛋白-2（MMRN2）在乳腺癌中的表达及对预后的影响，探讨其在乳腺癌发病机制中的作用。方法收集2013年1月~2017年4月在武汉大学人民医院行手术切除的乳腺浸润性导管癌标本和癌旁组织50例，采用Western blot和qRT-PCR检测MMRN2的表达情况，分析MMRN2表达量高低与患者病理特征及预后的关系。结果 MMRN2在乳腺癌组织中低表达（P < 0.01），MMRN2表达量高低与患者病理特征无明显相关性（P > 0.05），MMRN2高表达可以延长乳腺癌患者总生存期（P=0.036）和无复发生存期（P=0.019）。结论 MMRN2是乳腺癌的抑癌基因，可以作为一个潜在的乳腺癌分子治疗靶点，提高患者生存期。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	李华萍孙圣荣▲ 陈创汪媛

关键词 ：多聚蛋白-2, 乳腺癌, 抑癌基因, 预后

Abstract：Objective To investigate the expression of MMRN2 in breast cancer and its influence on prognosis, discuss the mechanism of MMRN2 in breast cancer. Methods Western blot and qRT-PCR were used to detect the expression of MMRN2 in 50 pairs of human breast invasive ductal carcinoma specimens and adjacent tissues, which had excision by surgery in Renmin Hospital of Wuhan University from January 2013 to April 2017. The relationship between the expression of MMRN2 and the pathologic features and prognosis of patients were analyzed. Results The expression of MMRN2 in breast cancer was down-regulated (P < 0.01), and the expression of MMRN2 was not correlated with the pathological characteristics of patients (P > 0.05). Up-regulated MMRN2 could prolong the overall survival (P = 0.036) and no recurrence survival time (P = 0.019) of patients with breast cancer. Conclusion MMRN2 is a tumor suppressor gene for breast cancer, and can serve as a potential target for molecular treatment of breast cancer, improve patients′ survival.

Key words： MMRN2 Breast cancer Anti-oncogene Prognosis

基金资助:国家自然科学基金资助项目（81471781）。

通讯作者: ▲通讯作者

引用本文:

李华萍孙圣荣▲ 陈创汪媛 . MMRN2在乳腺癌中的表达及对预后的影响[J]. 中国医药导报, 2017, 14(23): 4-7.
LI Huaping SUN Shengrong▲ CHEN Chuang WANG Yuan . Expression of MMRN2 in breast cancer and its influence on prognosis. 中国医药导报, 2017, 14(23): 4-7.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2017/V14/I23/4

[1] Beretov J，Wasinger VC，Graham PH，et al. Proteomics for breast cancer urine biomarkers [J]. Adv Clin Chem，2014， 63：123-167.
[2] Siegel RL，Miller KD，Jemal A. Cancer statistics，2017 [J]. CA Cancer J Clin，2017，67（1）：7-30.
[3] Cancer Genome Atlas Network.Comprehensive molecular portraits of human breast tumours [J]. Nature，2012，490（7418）：61-70.
[4] Germain D. Estrogen carcinogenesis in breast cancer [J]. Edodocrinol Metab Clin North Am，2011，40（3）：473-484.
[5] Yang SN，Li FJ，Chen JM，et al. Kinetic Curve Type Assessment for Classification of Breast Lesions Using Dynamic Contrast-Enhanced MR Imaging [J]. PLoS One，2016， 1（4）：e0152827.
[6] Julia B，Valerie C，Ewan K，et al. Proteomic Analysis of Urine to Identify Breast Cancer Biomarker Candidates Using a Label-Free LC-MS/MS Approach [J]. PLoS One，2015， 10（11）：e0141876.
[7] Lei T，Zhao X，Jin S，et al. Discovery of Potential Bladder Cancer Biomarkers by Comparative Urine Proteomics and Analysis [J]. Clin Genitour Cancer，2013，11（1）：56-62.
[8] Hassanein M，Callison JC，Callaway-Lane C，et al. The state of molecular biomarkers for the early detection of lung cancer [J]. Cancer Prevention Res，2012，5（8）：992-1006.
[9] Beretov J，Wasinger VC，Graham PH，et al. Proteomics for breast cancer urine biomarkers [J]. Adv Clin Chem，2014， 63：123-167.
[10] Rao N，Lee YF，Ge RW. Novel endogenous angiogenesis inhibitors and their therapeutic potential [J]. Acta Pharmacot Sin，2015，36（10）：1177-1190.
[11] Lorenzon E，Colladel R，Andreuzzi E，et al. MULTIMERIN2 impairs tumor angiogenesis and growth by interfering with VEGF-A/VEGFR2 pathway [J]. Oncogene，2012，31（26）：3136-3147.
[12] Welch-Reardon KM，Ehsan SM，Wang K，et al. Angiogenic sprouting is regulated by endothelial cell expression of Slug [J]. J Cell Sci，2014，127（Pt 9）：2017-2018.
[13] Yuan BQ，Xian RH，Ma JF，et al. Isthmin inhibits glioma growth through antiangiogenesis in vivo [J]. J Neuro Oncol，2012，109（2）：245-252.
[14] Van Buul JD，Geerts D，Huveneers S. Rho GAPs and GEFs： controling switches in endothelial cell adhesion [J]. Cell Adh Migr，2014，8（2）：108-124.
[15] Noy PJ，Lodhia P，Khan K，et al. Blocking CLEC14A-MMRN2 binding inhibits sprouting angiogenesis and tumour growth [J]. Oncogene，2015，34（47）：5821-5831.
[16] Blanco R，Gerhardt H. VEGF and Notch in tip and stalk cell selection [J]. Cold Spring Harb Perspect Med，2013， 3（1）：a006569.
[17] Chang GH，Lay AJ，Ting KK，et al. ARHGAP18： an endogenous inhibitor of angiogenesis， limiting tip formation and stabilizing junctions [J]. Small GTPases，2014，5（3）：1-15.
[18] Baker M，Robinson SD，Lechertier T，et al. Use of the mouse aortic ring assay to study angiogenesis [J]. Nat Protoc，2011，7（1）：89-104.
[19] De Angelis JE，Lagendijk AK，Chen H，et al. Tmem2 regulates embryonic vegf Signaling by controlling hyaluronic acid turnover [J]. dev cell，2017，40（2）：123-136.
[20] Andreuzzi E，Colladel R，Pellicani R，et al. The angiostatic molecule multimerin 2 is processed by MMP-9 to allow sprouting angiogenesis [J]. Matr Biol，2017.DOI：10.1016/j.matbio.2017.04.002