Anti-leukemic activity of microRNA-26a in a chronic lymphocytic leukemia mouse model

Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ- TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel thera...

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Published inOncogene Vol. 36; no. 47; pp. 6617 - 6626
Main Authors D’Abundo, L, Callegari, E, Bresin, A, Chillemi, A, Elamin, B K, Guerriero, P, Huang, X, Saccenti, E, Hussein, E M A A, Casciano, F, Secchiero, P, Zauli, G, Calin, G A, Russo, G, Lee, L J, Croce, C M, Marcucci, G, Sabbioni, S, Malavasi, F, Negrini, M
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 23.11.2017
Nature Publishing Group
Subjects
631/67/1059/602
631/67/1990/283/1895
ADP-ribosyl Cyclase 1 - antagonists & inhibitors
ADP-ribosyl Cyclase 1 - genetics
Animals
Antibodies, Monoclonal, Murine-Derived - chemistry
Apoptosis
Apoptosis - drug effects
Care and treatment
Caspase
Caspase 7 - metabolism
Caspase-7
CD38 antigen
Cell Biology
Cell Line, Tumor
Chronic lymphocytic leukemia
Cyclin-dependent kinase
Cyclin-dependent kinase 6
Cyclin-Dependent Kinase 6 - genetics
Cyclin-dependent kinases
Development and progression
Down-Regulation
Drug Delivery Systems
Female
Gene expression
Gene Expression Regulation, Neoplastic
Genetic aspects
Health aspects
Human Genetics
Humans
Internal Medicine
Kinases
Leukemia
Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy
Leukemia, Lymphocytic, Chronic, B-Cell - genetics
Lipids - chemistry
Lymphatic leukemia
Mcl-1 protein
Medicine
Medicine & Public Health
Membrane Glycoproteins - antagonists & inhibitors
Membrane Glycoproteins - genetics
Mice
Mice, Transgenic
MicroRNA
MicroRNAs
MicroRNAs - administration & dosage
MicroRNAs - antagonists & inhibitors
MicroRNAs - therapeutic use
miRNA
Monoclonal antibodies
Myeloid Cell Leukemia Sequence 1 Protein - genetics
Nanoparticles
Nanoparticles - chemistry
Neoplasms, Experimental - drug therapy
Neoplasms, Experimental - genetics
Oncology
original-article
Poly(ADP-ribose) Polymerases - metabolism
Proto-Oncogene Proteins - genetics
Rodents
Transgenic mice
Italy
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Abstract Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ- TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.
AbstractList Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The E[mu]-TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis. Oncogene (2017) 36, 6617-6626; doi: 10.1038/onc.2017.269; published online 7 August 2017
Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ-TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.
Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The E[mu]-TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.
Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ- TCL1 transgenic mouse develops a form of leukemia that is similar to the aggressive type of human B-CLL, and this valuable model has been widely used for testing novel therapeutic approaches. Here, we adopted this model to investigate the potential effects of miR-26a, miR-130an and antimiR-155 in CLL therapy. Improved delivery of miRNA molecules into CLL cells was obtained by developing a novel system based on lipid nanoparticles conjugated with an anti-CD38 monoclonal antibody. This methodology has proven to be highly effective in delivering miRNA molecules into leukemic cells. Short- and long-term experiments showed that miR-26a, miR-130a and anti-miR-155 increased apoptosis after in vitro and in vivo treatment. Of this miRNA panel, miR-26a was the most effective in reducing leukemic cell expansion. Following long-term treatment, apoptosis was readily detectable by analyzing cleavage of PARP and caspase-7. These effects could be directly attributed to miR-26a, as confirmed by significant downregulation of its proven targets, namely cyclin-dependent kinase 6 and Mcl1. The results of this study are relevant to two distinct areas. The first is related to the design of a technical strategy and to the selection of CD38 as a molecular target on CLL cells, both consenting efficient and specific intracellular transfer of miRNA. The original scientific finding inferred from the above approach is that miR-26a can elicit in vivo anti-leukemic activities mediated by increased apoptosis.
Audience Academic
Author Secchiero, P
Calin, G A
Huang, X
Sabbioni, S
Saccenti, E
Zauli, G
Guerriero, P
Croce, C M
Elamin, B K
Marcucci, G
Callegari, E
Malavasi, F
Lee, L J
Hussein, E M A A
Russo, G
D’Abundo, L
Chillemi, A
Negrini, M
Bresin, A
Casciano, F
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28783166$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
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  start-page: 1334
  year: 2006
  ident: BFonc2017269_CR17
  publication-title: Blood
  doi: 10.1182/blood-2005-12-011213
  contributor:
    fullname: AJ Johnson
– volume: 62
  start-page: 237
  year: 2012
  ident: BFonc2017269_CR77
  publication-title: Cell biochem biophys
  doi: 10.1007/s12013-011-9263-8
  contributor:
    fullname: XQ Jia
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Snippet Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ- TCL1 transgenic mouse develops a...
Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The Eμ-TCL1 transgenic mouse develops a...
Dysregulation of microRNAs (miRNAs) plays an important role in the pathogenesis of chronic lymphocytic leukemia (CLL). The E[mu]-TCL1 transgenic mouse develops...
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StartPage 6617
SubjectTerms 631/67/1059/602
631/67/1990/283/1895
ADP-ribosyl Cyclase 1 - antagonists & inhibitors
ADP-ribosyl Cyclase 1 - genetics
Animals
Antibodies, Monoclonal, Murine-Derived - chemistry
Apoptosis
Apoptosis - drug effects
Care and treatment
Caspase
Caspase 7 - metabolism
Caspase-7
CD38 antigen
Cell Biology
Cell Line, Tumor
Chronic lymphocytic leukemia
Cyclin-dependent kinase
Cyclin-dependent kinase 6
Cyclin-Dependent Kinase 6 - genetics
Cyclin-dependent kinases
Development and progression
Down-Regulation
Drug Delivery Systems
Female
Gene expression
Gene Expression Regulation, Neoplastic
Genetic aspects
Health aspects
Human Genetics
Humans
Internal Medicine
Kinases
Leukemia
Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy
Leukemia, Lymphocytic, Chronic, B-Cell - genetics
Lipids - chemistry
Lymphatic leukemia
Mcl-1 protein
Medicine
Medicine & Public Health
Membrane Glycoproteins - antagonists & inhibitors
Membrane Glycoproteins - genetics
Mice
Mice, Transgenic
MicroRNA
MicroRNAs
MicroRNAs - administration & dosage
MicroRNAs - antagonists & inhibitors
MicroRNAs - therapeutic use
miRNA
Monoclonal antibodies
Myeloid Cell Leukemia Sequence 1 Protein - genetics
Nanoparticles
Nanoparticles - chemistry
Neoplasms, Experimental - drug therapy
Neoplasms, Experimental - genetics
Oncology
original-article
Poly(ADP-ribose) Polymerases - metabolism
Proto-Oncogene Proteins - genetics
Rodents
Transgenic mice
Title Anti-leukemic activity of microRNA-26a in a chronic lymphocytic leukemia mouse model
URI https://link.springer.com/article/10.1038/onc.2017.269
https://www.ncbi.nlm.nih.gov/pubmed/28783166
https://www.proquest.com/docview/1967374339
https://www.proquest.com/docview/2615529305
https://search.proquest.com/docview/1926980257
Volume 36
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