The application of aptamer 5TR1 in triple negative breast cancer target therapy
| Autor: | Shayang Luo, Ke-Jing Zhang, Shou-Man Wang, Fei-Yu Chen, Chun Hu, Na Luo |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Cell Survival Aptamer medicine.medical_treatment Triple Negative Breast Neoplasms Pharmacology Biochemistry Targeted therapy 03 medical and health sciences Mice 0302 clinical medicine Breast cancer Drug Delivery Systems Cell Line Tumor medicine Animals Humans Doxorubicin Viability assay skin and connective tissue diseases Cytotoxicity Molecular Biology Triple-negative breast cancer Cell Proliferation Chemotherapy business.industry Mucin-1 Cell Biology Aptamers Nucleotide medicine.disease Xenograft Model Antitumor Assays 030104 developmental biology 030220 oncology & carcinogenesis Female business medicine.drug |
| Zdroj: | Journal of cellular biochemistry. 119(1) |
| ISSN: | 1097-4644 |
| Popis: | Chemotherapy is one of the standard strategies for treatment of breast cancer. Adriamycin (Dox) is a first-line chemotherapy agent for breast cancer. However, the gastrointestinal reactions, myocardial toxicity and other side effects caused by Dox due to its un-specific cytotoxicity limit the clinical treatment effect. To address this need, aptamer has been regarded as an ideal target molecular carrier. In the present study, we selected an aptamer 5TR1 that can specifically bind to the MUC1 protein which has been regarded as an important tumor biomarker, as well as a potential target in anticancer therapies. Dox was loaded on the modified 5TR1-GC, which specifically targets breast cancer cell MDA-MB-231. Cell viability and apoptosis assays demonstrated that the 5TR1-GC-Dox exhibited target specificity of cytotoxicity in MDA-MB-231. Moreover, in vivo xenograft study also confirmed that 5TR1-GC-Dox had a more effective effect on tumor growth inhibition and induced the apoptosis of malignant tumor cells compared to Dox. We provided a novel experimental and theoretical basis for developing an aptamer targeted drug system, thus to promote the killing effect of drugs on breast cells and to reduce the damage to normal cells and tissues for breast cancer. |
| Databáze: | OpenAIRE |
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