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PTD modified paclitaxel anti-resistant liposomes for treatment of drug-resistant non-small cell lung cancer.
Journal of Liposome Research 2018 September
CONTEXT: Non-small cell lung carcinoma (NSCLC) is a type of epithelial lung cancer that accounts for approximately 80-85% of lung carcinoma cases. Chemotherapy for the NSCLC is unsatisfactory due to multidrug resistance, nonselectively distributions and the accompanying side effects.
OBJECTIVE: The objective of this study was to develop a kind of PTD modified paclitaxel anti-resistant liposomes to overcome these chemotherapy limitations.
METHOD: The studies were performed on LLT cells and resistant LLT cells in vitro and on NSCLC xenograft mice in vivo, respectively.
RESULTS AND DISCUSSION: In vitro results showed that the liposomes with suitable physicochemical characteristics could significantly increase intracellular uptake in both LLT cells and resistant LLT cells, evidently inhibit the growth of cancer cells, and clearly induce the apoptosis of resistant LLT cells. Studies on resistant LLT cells xenograft mice demonstrated that the liposomes magnificently enhanced the anticancer efficacy in vivo. Involved action mechanisms were down-regulation of adenosine triphosphate binding cassette transporters on resistant LLT cells, and activation of the apoptotic enzymes (caspase 8/9/3).
CONCLUSION: The PTD modified paclitaxel anti-resistant liposomes may provide a promising strategy for treatment of the drug-resistant non-small cell lung cancer.
OBJECTIVE: The objective of this study was to develop a kind of PTD modified paclitaxel anti-resistant liposomes to overcome these chemotherapy limitations.
METHOD: The studies were performed on LLT cells and resistant LLT cells in vitro and on NSCLC xenograft mice in vivo, respectively.
RESULTS AND DISCUSSION: In vitro results showed that the liposomes with suitable physicochemical characteristics could significantly increase intracellular uptake in both LLT cells and resistant LLT cells, evidently inhibit the growth of cancer cells, and clearly induce the apoptosis of resistant LLT cells. Studies on resistant LLT cells xenograft mice demonstrated that the liposomes magnificently enhanced the anticancer efficacy in vivo. Involved action mechanisms were down-regulation of adenosine triphosphate binding cassette transporters on resistant LLT cells, and activation of the apoptotic enzymes (caspase 8/9/3).
CONCLUSION: The PTD modified paclitaxel anti-resistant liposomes may provide a promising strategy for treatment of the drug-resistant non-small cell lung cancer.
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