Differential uptake, kinetics and mechanisms of intracellular trafficking of next-generation antisense oligonucleotides across human cancer cell lines.


Journal

Nucleic acids research
ISSN: 1362-4962
Titre abrégé: Nucleic Acids Res
Pays: England
ID NLM: 0411011

Informations de publication

Date de publication:
21 05 2019
Historique:
accepted: 18 03 2019
revised: 11 03 2019
received: 20 12 2018
pubmed: 31 3 2019
medline: 22 11 2019
entrez: 31 3 2019
Statut: ppublish

Résumé

Antisense oligonucleotides (ASOs) modulate cellular target gene expression through direct binding to complementary RNA. Advances in ASO chemistry have led to the development of phosphorothioate (PS) ASOs with constrained-ethyl modifications (cEt). These next-generation cEt-ASOs can enter cells without transfection reagents. Factors involved in intracellular uptake and trafficking of cEt-ASOs leading to successful target knockdown are highly complex and not yet fully understood. AZD4785 is a potent and selective therapeutic KRAS cEt-ASO currently under clinical development for the treatment of cancer. Therefore, we used this to investigate mechanisms of cEt-ASO trafficking across a panel of cancer cells. We found that the extent of ASO-mediated KRAS mRNA knockdown varied significantly between cells and that this did not correlate with bulk levels of intracellular accumulation. We showed that in cells with good productive uptake, distribution of ASO was perinuclear and in those with poor productive uptake distribution was peripheral. Furthermore, ASO rapidly trafficked to the late endosome/lysosome in poor productive uptake cells compared to those with more robust knockdown. An siRNA screen identified several factors mechanistically involved in productive ASO uptake, including the endosomal GTPase Rab5C. This work provides novel insights into the trafficking of cEt-ASOs and mechanisms that may determine their cellular fate.

Identifiants

pubmed: 30927008
pii: 5423608
doi: 10.1093/nar/gkz214
pmc: PMC6511877
doi:

Substances chimiques

KRAS protein, human 0
Oligonucleotides, Antisense 0
Phosphorothioate Oligonucleotides 0
RNA, Messenger 0
RNA, Small Interfering 0
RAB5C protein, human EC 3.6.1.-
Proto-Oncogene Proteins p21(ras) EC 3.6.5.2
rab5 GTP-Binding Proteins EC 3.6.5.2

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

4375-4392

Subventions

Organisme : Medical Research Council
ID : MR/P01058X/1
Pays : United Kingdom

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press on behalf of Nucleic Acids Research.

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Auteurs

Emily Linnane (E)

Bioscience, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB10 1XL, UK.

Paul Davey (P)

Chemistry, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB4 0WG, UK.

Pei Zhang (P)

Bioscience, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB10 1XL, UK.

Sanyogitta Puri (S)

Advanced Drug Delivery, Pharmaceutical Sciences, IMED Biotech Unit, AstraZeneca, Cambridge, CB21 6GH, UK.

Mark Edbrooke (M)

Bioscience, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB10 1XL, UK.

Elisabetta Chiarparin (E)

Chemistry, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB4 0WG, UK.

Alexey S Revenko (AS)

Ionis Pharmaceuticals, Carlsbad, CA 92010, USA.

A Robert Macleod (AR)

Ionis Pharmaceuticals, Carlsbad, CA 92010, USA.

Jim C Norman (JC)

Cancer Research UK Beatson Institute, Glasgow, G61 1BD, UK.
Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1QH, UK.

Sarah J Ross (SJ)

Bioscience, Oncology, IMED Biotech Unit, AstraZeneca, Cambridge, CB10 1XL, UK.

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Classifications MeSH