摘要
细胞黏附分子CD44抗原与乳腺癌化疗耐药密切相关。其高表达能显著增强乳腺癌侵袭能力。CD44主要通过影响细胞转化生长因子-β（TGF-β）表达来促进乳腺癌细胞对三苯氧胺产生耐药性，而对erbB-2信号通路的调节是CD44影响乳腺癌曲妥珠单抗耐药的重要方式。通过诱导多药耐药相关蛋白（MRP）2上调及对拓扑异构酶Ⅱ的抑制，CD44加强了乳腺癌对蒽环类药物的耐药。而对survivn蛋白及多药耐药基因的调节增强了乳腺癌对紫杉类药物的耐药性。
The cell adhesion molecule CD44 antigen correlates with the antineoplastic agents resistance of breast neoplasms closely. Its high expression can enhance the invasion of the breast neoplasms. CD44 molecule can affect the expression of the TGF- β of breast neoplasm cells to induce the resistance to tamoxifen. The influence on erbB-2 cell signal pathway result in the resistance to the trastuzumab. CD44 can strengthen the resistance to anthracene nucleus by inducing expression of protein MRF2 and inhibiting the topoismerase. The modulation of survivn and muhidrug resistance gene intensifies the resistance to paclitaxel.
出处
《国际肿瘤学杂志》
CAS
2009年第7期521-524,共4页
Journal of International Oncology
关键词
抗原
CD44
乳腺肿瘤
抗药性
肿瘤
Antigens, CD44
Breast neoplasms
Drug resistance, neoplasm
