The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Antisense Inhibition of microRNA-21 or -221 Arrests Cell Cycle, Induces Apoptosis, and Sensitizes the Effects of Gemcitabine in Pancreatic Adenocarcinoma
Abstract
OBJECTIVES: The contribution of overexpressed microRNA-21 and -221 (miR-21 and miR-221) to the malignant phenotype was determined by inhibiting these miRNAs using antisense oligonucleotides. METHODS: The effects of antisense to miR-21 and miR-221 on cell proliferation, cell cycle arrest, induction of apoptosis, combinatorial effects with gemcitabine, and effects on target protein levels were studied. RESULTS: Low nanomolar concentrations of both antisense oligonucleotides reduced proliferation of pancreatic cancer cell lines. Reduced proliferation was less pronounced in the normal ductal epithelial cell line human pancreatic Nestin-expressing cell or in pancreatic cancer cell lines exposed to an irrelevant control oligonucleotide. Inhibition of miR-21 and miR-221 increased the amount of apoptosis in HS766T cells by 3- to 6-fold compared with the control oligonucleotide. HS766T cells exposed to miR-21 antisense resulted in cell cycle arrest (G1 phase). Protein levels of tumor suppressor targets of the miRNAs were increased by antisense to miR-21 (PTEN and RECK) and miR-221 (p27). Antisense to miR-21 and miR-221 sensitized the effects of gemcitabine, and the antisense-gemcitabine combinations were synergistic at high fraction affected. CONCLUSIONS: We demonstrate that antisense to miR-21 and miR-221 results in significant cell killing under various conditions and that antisense oligonucleotides targeted to miRNA represents a potential new therapy for pancreatic cancer.
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Metadata
- Authors
- Park, J.-K., Lee, E. J., Esau, C., & Schmittgen, T. D.
- Venue
- Pancreas
- Published
- 2009-10
- Volume
- 38
- Issue
- 7
- Pages
- e190-e199
- ISSN
- 0885-3177 (ISSN-L)
- OpenAlex
- W2026468262
- Cited by
- 287
- References
- 13
- FWCI
- 8.26
- Type
- journal article
- Language
- en
- Open access
- closed
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