长链非编码RNA HEIH通过负调控microRNA-200b促进乳腺癌的发展。

Jie Zhao, R. Meng, Q. Yao, Hui Wang, J. Niu, Y. Cui, Songlin Chen, Yin-Shan Bai
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引用次数: 11

摘要

本研究旨在探讨长链非编码RNA heh在乳腺癌发生发展中的作用及其调控机制。检测乳腺肿瘤组织和乳腺癌细胞中HEIH的表达,探讨HEIH失调对乳腺癌细胞活力、凋亡、迁移和侵袭的影响及其调控机制。在乳腺癌组织样本和细胞系中,HEIH的表达上调。抑制heh抑制MDA-MB-231细胞活力,促进细胞凋亡,减少细胞迁移和侵袭。此外,heh与miR-200b之间存在负相关关系,heh通过调节miR-200b调节乳腺癌的发展。白血病前转录因子3 (Pre-leukemia transcription factor 3, PBX3)被证实是miR-200b的功能靶点,miR-200b通过靶向PBX3调节乳腺癌细胞的恶性行为。此外,抑制HEIH抑制Wnt/β-catenin通路的激活,在抑制HEIH和抑制miR-200b同步后,Wnt/β-catenin通路的激活被显著逆转。我们的研究结果表明,heh可能通过调节microRNA-200b/轴和诱导Wnt/β-catenin通路的激活来促进乳腺癌的发展。还需要进一步的研究来证实我们的发现。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long non-coding RNA HEIH promotes breast cancer development via negative modulation of microRNA-200b.
This study aimed to investigate the effects and regulatory mechanism of long non-coding RNA HEIH in the development of breast cancer. The expression of HEIH in breast tumor tissues and breast cancer cells was determined, followed by investigating the effects and regulatory mechanism of HEIH dysregulation on breast cancer cell viability, apoptosis, migration and invasion. The expression of HEIH was upregulated in breast cancer tissue samples and cell lines. Suppression of HEIH inhibited cell viability, promoted cell apoptosis, and decreased migration and invasion in MDA-MB-231 cells. Moreover, a negative relationship existed between HEIH and miR-200b, and HEIH regulated breast cancer development via regulating miR-200b. Pre-leukemia transcription factor 3 (PBX3) was verified as a functional target of miR-200b, and miR-200b regulated the malignant behaviors of breast cancer cells through targeting PBX3. Furthermore, suppression of HEIH inhibited the activation of Wnt/β-catenin pathway, which was remarkably reversed after suppression of HEIH and inhibition of miR-200b synchronously. Our results reveal that HEIH may contribute to breast cancer development via modulation of microRNA-200b/axis and inducing the activation of Wnt/β-catenin pathway. Further studies are still required to confirm our findings.
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