Results
CSC Numbers Are Increased in Breast Cancer Cells Induced into an EMT
We sought to increase the proportion of CSCs in breast cancer cell populations by inducing them to pass through an EMT. To this end, we modified experimentally transformed HMLER breast cancer cells (Elenbaas et al., 2001) by short hairpin RNA (shRNA)-mediated inhibition of the human CDH1 gene, which encodes E-cadherin. Confirming previous results, an shEcad vector triggered an EMT and resulted in acquisition of a mesenchymal phenotype (Figure 1A) (Onder et al., 2008). Moreover, expression of a murine E-cadherin gene resistant to the introduced human shEcad construct caused reversion of EMT-associated phenotypes, indicating that EMT induction was not due to off-target shRNA effects (Figure 1A).
ResultsCSC Numbers Are Increased in Breast Cancer Cells Induced into an EMTWe sought to increase the proportion of CSCs in breast cancer cell populations by inducing them to pass through an EMT. To this end, we modified experimentally transformed HMLER breast cancer cells (Elenbaas et al., 2001) by short hairpin RNA (shRNA)-mediated inhibition of the human CDH1 gene, which encodes E-cadherin. Confirming previous results, an shEcad vector triggered an EMT and resulted in acquisition of a mesenchymal phenotype (Figure 1A) (Onder et al., 2008). Moreover, expression of a murine E-cadherin gene resistant to the introduced human shEcad construct caused reversion of EMT-associated phenotypes, indicating that EMT induction was not due to off-target shRNA effects (Figure 1A).
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