AI Article Synopsis
- Multidrug resistance (MDR) in cancer involves various mechanisms that allow cancer cells to resist multiple chemotherapy drugs, including P-glycoprotein activity and the overexpression of inhibitors of apoptosis proteins.
- MDR can be spread to sensitive cancer cells through membrane microparticles (MP) derived from MDR-positive cells, leading to the accumulation of resistance-related proteins and genetic material in these sensitive cells.
- Co-culturing MDR-positive MP with sensitive cells resulted in enhanced activation of key pathways, suggesting that MP play a significant role in converting vulnerable cancer cells into more resistant ones.
Article Abstract
Multidrug resistance (MDR) is considered a multifactorial event that favors cancer cells becoming resistant to several chemotherapeutic agents. Numerous mechanisms contribute to MDR, such as P-glycoprotein (Pgp/ABCB1) activity that promotes drug efflux, overexpression of inhibitors of apoptosis proteins (IAP) that contribute to evasion of apoptosis, and oncogenic pathway activation that favors cancer cell survival. MDR molecules have been identified in membrane microparticles (MP) and can be transferred to sensitive cancer cells. By co-culturing MP derived from MDR-positive cells with recipient cells, we showed that sensitive cells accumulated Pgp, IAP proteins and mRNA. In addition, MP promoted microRNA transfer and NFκB and Yb-1 activation. Therefore, our results indicate that MP can induce a multifactorial phenotype in sensitive cancer cells.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4317771 | PMC |
| http://dx.doi.org/10.1111/cas.12566 | DOI Listing |
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