腫瘤轉(zhuǎn)移相關(guān)基因家族是近年發(fā)現(xiàn)的由某些腫瘤轉(zhuǎn)移相關(guān)基因及其編碼產(chǎn)物組成的家族,而作為該家族中首個被發(fā)現(xiàn)的基因,轉(zhuǎn)移性腫瘤抗原1（metastatic tumor antigen 1，MTA1）基因在多種惡性腫瘤中過度表達(dá)，并且與人類腫瘤的惡性特征密切相關(guān),。
MTA1基因在乳腺的激素調(diào)控和乳腺癌的發(fā)生、發(fā)展中都起到了重要的作用,，因此MTA1基因及其編碼蛋白的檢測可能成為乳腺癌新的臨床預(yù)后指標(biāo)和治療靶點(diǎn)。
轉(zhuǎn)移腫瘤抗原1（MTA1）是一個潛在的轉(zhuǎn)移相關(guān)候選基因,，在體外,，MTA1的增加導(dǎo)致各種類型腫瘤細(xì)胞的遷移和侵襲增加。此外,，MTA1還在腫瘤的發(fā)生和侵襲性乳腺癌腫瘤中起著重要作用,。
雌激素受體α（甲型雌激素受體）在乳腺癌發(fā)病中扮演重要作用，已被廣泛證實(shí)是乳腺癌的預(yù)后指標(biāo),。近日,，Tumor Biology雜志上的一則研究評估了雌激素受體甲型甲基化和MTA1表達(dá)在乳腺癌中的作用，進(jìn)一步研究分析抑制雌激素受體甲型甲基化是否可以下調(diào)MTA1的表達(dá),。聚合酶鏈反應(yīng)和免疫組化研究發(fā)現(xiàn),，乳腺癌女性患者中雌激素受體甲型甲基化與MTA1表達(dá)甲基化特異性有顯著相關(guān)性。這些數(shù)據(jù)有力地支持了甲基化參與乳腺癌MTA1和雌激素受體甲型之間的相互作用,。（生物谷：Bioon.com）
doi:10.1007/s13277-012-0410-7
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MTA1 expression correlates significantly with ER-alpha methylation in breast cancer
Xiao-yun Mao, Hao Chen, Huan Wang, Jing Wei, Chong Liu, Hua-chuan Zheng, Fan Yao and Feng Jin
Metastasis tumor antigen 1 (MTA1), a novel candidate metastasis-associated gene, is known to increase the migration and invasion of various tumor cells in vitro. It also plays an important role in tumorigenesis and tumor aggressiveness of breast cancer. Estrogen receptor alpha (ERα) plays an important role in the etiology of breast cancer and has been widely accepted as a prognostic marker for breast cancer and a response predictor for endocrine therapy. The ERα gene methylation has been linked to the lack of ERα expression in breast cancer. The aim of the study is to assess the correlation between the ERα methylation and MTA1 expression in breast cancer and further to investigate whether the repressed ERα methylation can downregulate the expression of MTA1 in vitro. In general, we found ERα methylation had significant correlation with the MTA1 expression (p < 0.05) in female patients of breast cancer (n = 102) by methylation-specific polymerase chain reaction and immunohistochemistry. To gain a deeper insight into the molecular mechanism underlying the relation between MTA1 and ERα methylation, we treated the invasive breast cancer cell lines with the demethylating agent, found the downregulation of MTA1 protein expression, and mRNA with the unmethylation of ERα (p < 0.05). And the invasive ability of breast cancer cells was significantly positively associated with MTA1 expression. These unique findings have greatly extended our current knowledge about the relation between ERα methylation and MTA1 expression. These data strongly support the hypothesis that methylation is involved in the relation between MTA1 and ERα in breast cancer.
