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Most triple-negative breast cancers (TNBCs) are highly malignant and resistant to chemotherapy. Because TNBCs do not express estrogen receptor (ERa) and human epidermal growth factor receptor 2 (HER2), the currently available therapies that target estrogen and HER2 signaling pathways are not applicable for TNBC treatment. Twist is frequently expressed in TNBC cells and it has been shown to promote epithelial mesenchymal transition (EMT), migration, invasion, metastasis and survival of many types of cancer cells. To define the specific role of Twist in TNBC cells, we generated MDA-231LM3.3 cells expressing either non-targeting shRNAs or Twist mRNA-targeting shRNAs and analyzed the effects of Twist silencing on the viability, behavior and chemoresistance of these cells. We found that knockdown of Twist in MDA-231LM3.3 TNBC cells significantly decreased their colony formation capability and increased their apoptosis rate. Furthermore, knockdown of Twist in these cells also significantly inhibited their migration and invasion capabilities and elevated their sensitivities to breast cancer chemotherapeutic drugs including Cisplatin, Docorubicin and Vinorelbine. These results indicate that Twist is required for the viability, migration, invasion and chemoresistance of MDA-231LM3.3 cells, suggesting that Twist may serve as a molecular target for controlling certain TNBCs.
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