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首页> 外文期刊>Cellular Physiology and Biochemistry >Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition
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Silencing of Prrx2 Inhibits the Invasion and Metastasis of Breast Cancer both In Vitro and In Vivo by Reversing Epithelial-Mesenchymal Transition

机译：沉默Prrx2通过逆转上皮-间充质转化抑制乳腺癌的侵袭和转移。

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>Background/Aims: Epithelial-mesenchymal transition (EMT) is recognized as a crucial mechanism in breast cancer progression and metastasis. Paired-related homeobox 2 (Prrx2) has been identified as a new EMT inducer in cancer, but the underlying mechanisms are still poorly understood. Methods: The expression of Prrx2 was assessed by immunohistochemistry in breast cancer tissues to evaluate the clinicopathological significance of Prrx2, as well as the correlation between Prrx2 and EMT. Short hairpin RNA knockdown of Prrx2 was used to examine cellular effects of Prrx2, detecte the expression of Wnt/?2-catenin signaling and EMT-associated proteins, and observe cell proliferation, invasion and migration abilities in vitro and in vivo. Results: Clinical association studies showed that Prrx2 expression was related to tumor size, lymph node metastasis, tumor node metastasis stages, EMT and poor survival. Results also showed that knockdown of Prrx2 could alter cell morphology, suppressed the abilities of cell proliferation, invasion and migration in breast cancer. Moreover, silencing of Prrx2 induced the mesenchymal-epithelial transition and prevented nuclear translocation of ?2-catenin, inhibited wnt/?2-catenin signaling pathway. Conclusion: Our study indicated that Prrx2 may be an important activator of EMT in human breast cancer and it can serve as a molecular target of therapeutic interventions for breast cancer.
机译：> 背景/目标： 上皮-间质转化（EMT）被认为是乳腺癌进展和转移的关键机制。配对相关的同源盒2（Prrx2）已被确定为癌症中一种新的EMT诱导剂，但其潜在机制仍知之甚少。 方法： 采用免疫组织化学方法检测乳腺癌组织中Prrx2的表达，以评价Prrx2的临床病理意义以及Prrx2与EMT的相关性。使用Prrx2的短发夹RNA敲低来检查Prrx2的细胞作用，检测Wnt /α2-catenin信号和EMT相关蛋白的表达，并观察细胞的增殖，侵袭和迁移能力 和体内。 结果： 临床关联研究表明Prrx2表达与肿瘤大小，淋巴结转移，肿瘤结点转移阶段，EMT和不良生存率有关。结果还表明，敲低Prrx2可以改变细胞形态，抑制乳腺癌细胞的增殖，侵袭和迁移能力。此外，Prrx2的沉默诱导间充质-上皮转化，并阻止了β2-catenin的核易位，抑制了wnt /β2-catenin信号通路。 结论： 我们的研究表明Prrx2可能是人类乳腺癌中EMT的重要激活剂，并且可以作为乳腺癌治疗干预的分子靶标。

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