ArticleJournal of cellular physiology2012
Mechanism of T-oligo-induced cell cycle arrest in Mia-PaCa pancreatic cancer cells.
Article in Journal of cellular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Telomeric autophagy in human health, aging, and diseases.Frontiers in molecular biosciences · 2026Review
- Oligonucleotides Targeting Telomeres and Telomerase in Cancer.Molecules (Basel, Switzerland) · 2018Review
- Site specific replacements of a single loop nucleoside with a dibenzyl linker may switch the activity of TBA from anticoagulant to antiproliferative.Nucleic acids research · 2015Article
- Article
- T-oligo as an anticancer agent in colorectal cancer.Biochemical and biophysical research communications · 2014Article
- Non-small cell lung cancer is susceptible to induction of DNA damage responses and inhibition of angiogenesis by telomere overhang oligonucleotides.Cancer letters · 2014Article
- Novel delivery system for T-oligo using a nanocomplex formed with an alpha helical peptide for melanoma therapy.International journal of nanomedicine · 2014Article
- Enhanced cytotoxicity from deoxyguanosine-enriched T-oligo in prostate cancer cells.Nucleic acid therapeutics · 2013Article
- Telomere-homologous G-rich oligonucleotides sensitize human ovarian cancer cells to TRAIL-induced growth inhibition and apoptosis.Nucleic acid therapeutics · 2013Article
- Mechanism of DNA damage responses induced by exposure to an oligonucleotide homologous to the telomere overhang in melanoma.Oncotarget · 2013Article
- hnRNP C1/C2 and Pur-beta proteins mediate induction of senescence by oligonucleotides homologous to the telomere overhang.OncoTargets and therapy · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DNA oligonucleotides with sequence homology to human telomeric DNA (T-oligo) induce cell cycle arrest, followed by apoptosis, senescence, or autophagy in a human cancer cell type-specific manner. T-oligo has potential as a new therapeutic strategy in oncology because of its ability to target certain types of tumor cells while sparing normal ones. In the present study, we demonstrate the T-oligo-induced S-phase cell cycle arrest in four pancreatic cancer cell lines. To further contribute to the mechanistic understanding of T-oligo, we also identify cyclin dependent kinase 2 (cdk2) as a functional mediator in the T-oligo-induced cell cycle arrest of pancreatic cancer cells. Ectopic expression of a constitutively active cdk2 mutant abrogates T-oligo-induced cell cycle arrest in these tumor cells while knockdown of cdk2 expression alone recapitulates the T-oligo effect. Finally, we demonstrate the dispensability of T-oligo-induced ATM/ATR-mediated DNA damage response-signaling pathways, which have long been considered functional in the T-oligo signaling mechanism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.