Abstract
In order to eliminate common side effects to cancer patients and resistance from chemotherapy, a genetic protein TmSm(T34A) was investigated as a sensitizer to doxorubicin. The results indicated TmSm(T34A) enhanced the sensitivity of three breast cancer cell lines to doxorubicin with low dose, and reduced the dose of doxorubicin significantly in contrast to common effective dose. As a synergistic therapy, the TmSm(T34A) also caused strongest apoptotic activity in MCF-7, and the possible molecular mechanisms were explored primarily. The research showed the TmSm(T34A) is promising to be a potential drug in strengthening therapy effects of breast cancer chemotherapy.
Copyright © 2012 Elsevier Masson SAS. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antibiotics, Antineoplastic / administration & dosage
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Antibiotics, Antineoplastic / pharmacology
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Apoptosis / drug effects
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Apoptosis Regulatory Proteins / administration & dosage
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Apoptosis Regulatory Proteins / pharmacology*
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Breast Neoplasms / drug therapy*
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Breast Neoplasms / pathology
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Cell Line, Tumor
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Dose-Response Relationship, Drug
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Doxorubicin / administration & dosage
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Doxorubicin / pharmacology*
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Drug Resistance, Neoplasm / drug effects
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Drug Synergism
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Female
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Humans
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Recombinant Fusion Proteins / administration & dosage
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Recombinant Fusion Proteins / pharmacology*
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Survivin
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tat Gene Products, Human Immunodeficiency Virus / administration & dosage
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tat Gene Products, Human Immunodeficiency Virus / pharmacology*
Substances
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Antibiotics, Antineoplastic
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Apoptosis Regulatory Proteins
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HIV-TAT-survivin (T34A) protein
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Recombinant Fusion Proteins
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Survivin
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tat Gene Products, Human Immunodeficiency Virus
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Doxorubicin