PO.MCB10.01 · 分子与细胞生物学
miR-1260a促进乳腺癌的增殖和迁移
miR-1260a promotes proliferation and migration in breast cancer
作者与单位 Authors & Affiliations
摘要 Abstract
中文摘要
背景:microRNA(miRNA)调控细胞和病理过程,包括癌症。正如我们团队此前所述,miR-1260a在乳腺癌组织中上调。本研究的目的是在乳腺癌模型中表征miR-1260a。
方法:通过RNA芯片和qRT-PCR在乳腺癌患者中研究miR-1260a水平。利用增殖实验、集落形成实验、蛋白质印迹、RT-qPCR和免疫组织化学,研究了miR-1260a介导乳腺癌细胞生长、侵袭及其靶蛋白的作用和机制。
结果:在此,我们发现在一个包含50例乳腺癌患者的临床数据库中,miR-1260a表达在luminal B型肿瘤中最高,其次为三阴性肿瘤和luminal A型肿瘤。此外,miR-1260a表达与cyclin D1蛋白呈正相关。另一方面,过表达miR-1260a促进了MCF7、MDA-MB-231、MDA-MB-468和T47D细胞的增殖。此外,miR-1260a诱导MCF7和MDA-MB-231细胞的侵袭。而且,我们的结果表明,miR-1260a的致癌特性与GCDH和ERP29的抑制相关,这两种抑癌蛋白在乳腺癌中下调。
结论:这些发现表明miR-1260a促进了癌细胞的致癌特性,可能作为激素依赖型(luminal A和B)以及三阴性乳腺癌的一个新的潜在治疗靶点。
查看英文原文 English abstract
Background: MicroRNAs (miRNAs) regulate cellular and pathological processes, including cancer. As previously described by our group, miR-1260a was upregulated in breast cancer tissue. The aim of this research was to characterize miR-1260a in the breast cancer model.
Methods: MiR-1260a levels were studied by RNA array and qRT-PCR in breast cancer patients. The role and mechanisms underlying miR-1260a-mediated breast cancer cell growth, invasion and target proteins were studied using proliferation assays, colony formation assays, western blot, RT-qPCR and immunohistochemistry.
Results: Here, we found that miR-1260a expression is higher in luminal B tumors, followed by triple-negative tumors, and luminal A tumors in a clinical database of 50 breast cancer patients. Moreover, miR-1260a expression correlates positively with cyclin D1 protein. On the other hand, miR-1260a overexpression promotes the proliferation of MCF7, MDA-MD-231, MDA-MB-468, and T47D cells. In addition, miR-1260a induces the invasion of MCF7 and MDA-MB-231 cells. Moreover, our results suggest that the oncogenic properties of miR-1260a are linked to GCDH and ERP29 inhibition, two tumor suppressor proteins downregulated in breast cancer.
Conclusion: These findings indicate that miR-1260a promotes the oncogenic properties of cancer cells and may be useful as a new potential therapeutic target in hormone-dependent (luminal A and B) and triple-negative breast cancer.
利益披露 Disclosure
M. Bataller, None..
A. Feliciano, None..
Y. Sun, None..
D. Gala, None..
M. Biasini, None..
A. Sánchez-García, None..
C. Mir, None..
J. Castellvi, None..
S. Benavente, None..
Y. García-Mayea, None..
M. E. LLeonart Pajarín, None.