Sequential treatment of drug-resistant tumors with targeted minicells containing siRNA or a cytotoxic drug

Drug resistance remains a major hurdle to effective cancer chemotherapy. MacDiarmid et al . show that bacterially derived minicells packaged with siRNAs reverse tumor drug resistance and that subsequent treatment with minicells loaded with cytotoxic drugs causes tumor stabilization or regression. Th...

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Published inNature biotechnology Vol. 27; no. 7; pp. 643 - 651
Main Authors Brahmbhatt, Himanshu, MacDiarmid, Jennifer A, Amaro-Mugridge, Nancy B, Madrid-Weiss, Jocelyn, Sedliarou, Ilya, Wetzel, Stefanie, Kochar, Kartini, Brahmbhatt, Vatsala N, Phillips, Leo, Pattison, Scott T, Petti, Carlotta, Stillman, Bruce, Graham, Robert M
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.07.2009
Nature Publishing Group
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Abstract Drug resistance remains a major hurdle to effective cancer chemotherapy. MacDiarmid et al . show that bacterially derived minicells packaged with siRNAs reverse tumor drug resistance and that subsequent treatment with minicells loaded with cytotoxic drugs causes tumor stabilization or regression. The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose daunting challenges to effective cancer therapy. We report that small interfering RNA (siRNA) duplexes readily penetrate intact bacterially derived minicells previously shown to cause tumor stabilization and regression when packaged with chemotherapeutics. When targeted via antibodies to tumor-cell-surface receptors, minicells can specifically and sequentially deliver to tumor xenografts first siRNAs or short hairpin RNA (shRNA)–encoding plasmids to compromise drug resistance by knocking down a multidrug resistance protein. Subsequent administration of targeted minicells containing cytotoxic drugs eliminate formerly drug-resistant tumors. The two waves of treatment, involving minicells loaded with both types of payload, enable complete survival without toxicity in mice with tumor xenografts, while involving several thousandfold less drug, siRNA and antibody than needed for conventional systemic administration of cancer therapies.
AbstractList The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose daunting challenges to effective cancer therapy. We report that small interfering RNA (siRNA) duplexes readily penetrate intact bacterially derived minicells previously shown to cause tumor stabilization and regression when packaged with chemotherapeutics. When targeted via antibodies to tumor-cell-surface receptors, minicells can specifically and sequentially deliver to tumor xenografts first siRNAs or short hairpin RNA (shRNA)--encoding plasmids to compromise drug resistance by knocking down a multidrug resistance protein. Subsequent administration of targeted minicells containing cytotoxic drugs eliminate formerly drug-resistant tumors. The two waves of treatment, involving minicells loaded with both types of payload, enable complete survival without toxicity in mice with tumor xenografts, while involving several thousandfold less drug, siRNA and antibody than needed for conventional systemic administration of cancer therapies.
Drug resistance remains a major hurdle to effective cancer chemotherapy. MacDiarmid et al . show that bacterially derived minicells packaged with siRNAs reverse tumor drug resistance and that subsequent treatment with minicells loaded with cytotoxic drugs causes tumor stabilization or regression. The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose daunting challenges to effective cancer therapy. We report that small interfering RNA (siRNA) duplexes readily penetrate intact bacterially derived minicells previously shown to cause tumor stabilization and regression when packaged with chemotherapeutics. When targeted via antibodies to tumor-cell-surface receptors, minicells can specifically and sequentially deliver to tumor xenografts first siRNAs or short hairpin RNA (shRNA)–encoding plasmids to compromise drug resistance by knocking down a multidrug resistance protein. Subsequent administration of targeted minicells containing cytotoxic drugs eliminate formerly drug-resistant tumors. The two waves of treatment, involving minicells loaded with both types of payload, enable complete survival without toxicity in mice with tumor xenografts, while involving several thousandfold less drug, siRNA and antibody than needed for conventional systemic administration of cancer therapies.
The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose daunting challenges to effective cancer therapy. We report that small interfering RNA (siRNA) duplexes readily penetrate intact bacterially derived minicells previously shown to cause tumor stabilization and regression when packaged with chemotherapeutics. When targeted via antibodies to tumor-cell-surface receptors, minicells can specifically and sequentially deliver to tumor xenografts first siRNAs or short hairpin RNA (shRNA)-encoding plasmids to compromise drug resistance by knocking down a multidrug resistance protein. Subsequent administration of targeted minicells containing cytotoxic drugs eliminate formerly drug-resistant tumors. The two waves of treatment, involving minicells loaded with both types of payload, enable complete survival without toxicity in mice with tumor xenografts, while involving several thousandfold less drug, siRNA and antibody than needed for conventional systemic administration of cancer therapies. [PUBLICATION ABSTRACT]
Audience Academic
Author Madrid-Weiss, Jocelyn
Stillman, Bruce
Amaro-Mugridge, Nancy B
Brahmbhatt, Vatsala N
Sedliarou, Ilya
Wetzel, Stefanie
Phillips, Leo
Brahmbhatt, Himanshu
Petti, Carlotta
Kochar, Kartini
MacDiarmid, Jennifer A
Pattison, Scott T
Graham, Robert M
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IsPeerReviewed true
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Issue 7
Keywords Antineoplastic agent
Drug
Resistance
Delivery system
Gene silencing
RNA interference
Treatment
Targeting
Tumor
siRNA
Minicell
Cancer
Language English
License CC BY 4.0
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Snippet Drug resistance remains a major hurdle to effective cancer chemotherapy. MacDiarmid et al . show that bacterially derived minicells packaged with siRNAs...
The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose...
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StartPage 643
SubjectTerms Agriculture
Animals
Antineoplastic Agents - administration & dosage
Antineoplastic Agents - pharmacokinetics
ATP Binding Cassette Transporter, Subfamily B, Member 1 - biosynthesis
ATP Binding Cassette Transporter, Subfamily B, Member 1 - metabolism
Bioinformatics
Biological and medical sciences
Biomedical and Life Sciences
Biomedical Engineering/Biotechnology
Biomedicine
Biotechnology
Cancer
Care and treatment
Cell Cycle Proteins - genetics
Cell Line, Tumor
Cell- and Tissue-Based Therapy - methods
Cellular biology
Chemotherapy
Drug Delivery Systems - methods
Drug resistance
Drug Resistance, Multiple
Drug Resistance, Neoplasm
Drug therapy
Female
Fundamental and applied biological sciences. Psychology
Gene Knockdown Techniques
Genetic aspects
HCT116 Cells
Health. Pharmaceutical industry
Heterogeneity
Humans
Industrial applications and implications. Economical aspects
Life Sciences
Mice
Mice, Nude
Microscopy, Fluorescence
Miscellaneous
Neoplasms - drug therapy
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - therapy
Polo-Like Kinase 1
Protein Serine-Threonine Kinases - genetics
Proto-Oncogene Proteins - genetics
Ribonucleic acid
RNA
RNA, Small Interfering - administration & dosage
RNA, Small Interfering - genetics
Salmonella typhimurium - physiology
Toxicity
Tumors
Xenograft Model Antitumor Assays
Title Sequential treatment of drug-resistant tumors with targeted minicells containing siRNA or a cytotoxic drug
URI http://dx.doi.org/10.1038/nbt.1547
https://link.springer.com/article/10.1038/nbt.1547
https://www.ncbi.nlm.nih.gov/pubmed/19561595
https://www.proquest.com/docview/222235056
https://search.proquest.com/docview/20198478
Volume 27
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