目的 观察下调Ras同源类似物E (RhoE)表达对人乳腺癌细胞231生物学行为的影响。 方法 蛋白质印迹技术检测小干扰RNA（siRNA）转染前后RhoE在乳腺癌细胞231中的表达；RhoE siRNA的细胞转染 用lipofectamine?2000脂质体法；Cell Counting Kit-8检测转染细胞及对照细胞的增殖变化；损伤刮擦试验和体外侵袭实验（Transwell小室）分别检测转染细胞及对照细胞的迁移与侵袭能力。 结果 RhoE在乳腺癌细胞231中的表达较高；成功转染RhoE siRNA的乳腺癌细胞，蛋白质印迹显示RhoE的表达被明显的抑制；RhoE的表达被抑制后对乳腺癌细胞的增殖、迁移和侵袭有着明显的促进作用。 结论 下调RhoE 表达能够明显促进乳腺癌细胞的增殖﹑迁移和侵袭，RhoE可能在乳腺癌的发生发展中起着重要作用。
To aggressively proliferate and metastasize, cancer cells are in extreme need of energy supply and nutrients. Therefore, a promising cancer therapy strategy is developed to target its hallmark feature of metabolism. Recent findings revealed the regulatory role of caveolin-1 (Cav-1), a structural protein of caveolae, in cancer metabolism. And low Cav-1 expression in tumor stroma was proved to be a central player of cancer malignant phenotype. Here, we summarized the progressions of studies on Cav-1, mitochondria and cancer metabolism to indicate that the altered metabolism induced by Cav-1 and mitochondria association is a major cause of cancer malignant phenotype.