乳腺癌是最常见的癌症之一,也是女性癌症死亡的主要原因。MIER3(中胚层诱导早期反应1,家族成员3)被认为是乳腺癌的潜在癌基因。然而,MIER3在乳腺癌中的作用还不清楚.检测MIER3的表达,并分析其表达与临床病理特征的关系。在体外和体内检测MIER3对乳腺癌细胞增殖和迁移的影响。蛋白质印迹,如果,和Co-IP用于检测MIER3、HDAC1、HDAC2和蜗牛之间的关系。进行ChIP测定以确定MIER3/HDAC1/HDAC2/Snail复合物与E-钙粘蛋白启动子的结合。在这项研究中,我们发现MIER3在乳腺癌组织中上调,并与患者的不良预后密切相关.MIER3可以促进扩散,迁移,和乳腺癌细胞的上皮-间质转化(EMT)。进一步的研究表明,MIER3与HDAC1/HDAC2和Snail相互作用形成抑制复合物,该复合物可与E-cadherin启动子结合,并与其去乙酰化有关。我们的研究得出结论,MIER3参与与HDAC1/HDAC2/Snail形成共阻遏复合物,以通过沉默E-cadherin促进EMT。
Breast cancer is one of the most frequently diagnosed cancers and the leading cause of cancer death in women.
MIER3 (Mesoderm induction early response 1, family member3) is considered as a potential oncogene for breast cancer. However, the role of
MIER3 in breast cancer remain largely unknown. The expression of
MIER3 was detected and the relationship between its expression and clinicopathological characteristics was also analyzed. The effect of
MIER3 on proliferation and migration of breast cancer cells was detected in vitro and in vivo. Western blot, IF, and Co-IP were employed to detect the relationship between
MIER3, HDAC1, HDAC2, and Snail. ChIP assay was performed to determine the binding of MIER3/HDAC1/HDAC2/Snail complex to the promoter of E-cadherin. In this study, we found that MIER3 was upregulated in breast cancer tissue and closely associated with poor prognosis of patients. MIER3 could promote the proliferation, migration, and epithelial-mesenchymal transition (EMT) of breast cancer cells. Further studies showed that MIER3 interacted with HDAC1/HDAC2 and Snail to form a repressive complex which could bind to E-cadherin promoter and was related to its deacetylation. Our study concluded that MIER3 was involved in forming a co-repressor complex with HDAC1/HDAC2/Snail to promote EMT by silencing E-cadherin.