ArticleOncotarget2016
Identification of DNA-PKcs as a primary resistance factor of salinomycin in osteosarcoma cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Development and Evolution of DNA-Dependent Protein Kinase Inhibitors toward Cancer Therapy.International journal of molecular sciences · 2022Review
- Interactions between miRNAs and Double-Strand Breaks DNA Repair Genes, Pursuing a Fine-Tuning of Repair.International journal of molecular sciences · 2022Review
- MAFG-driven osteosarcoma cell progression is inhibited by a novel miRNA miR-4660.Molecular therapy. Nucleic acids · 2021Article
- AMPK activation by ASP4132 inhibits non-small cell lung cancer cell growth.Cell death & disease · 2021Article
- PF-06409577 Activates AMPK Signaling and Inhibits Osteosarcoma Cell Growth.Frontiers in oncology · 2021Article
- DNA-dependent protein kinase regulates lysosomal AMP-dependent protein kinase activation and autophagy.Autophagy · 2020Article
- Beta Human Papillomavirus 8E6 Attenuates Non-Homologous End Joining by Hindering DNA-PKcs Activity.Cancers · 2020Article
- Targeting autophagy is a promising therapeutic strategy to overcome chemoresistance and reduce metastasis in osteosarcoma.International journal of oncology · 2019Review
- NVP-BEZ235 synergizes cisplatin sensitivity in osteosarcoma.Oncotarget · 2018Article
- Salinomycin, as an autophagy modulator-- a new avenue to anticancer: a review.Journal of experimental & clinical cancer research : CR · 2018Review
- MiR-101: a potential therapeutic target of cancers.American journal of translational research · 2018Review
- SphK2 over-expression promotes osteosarcoma cell growth.Oncotarget · 2017Article
- Kaempferol induces autophagic cell death of hepatocellular carcinoma cells via activating AMPK signaling.Oncotarget · 2017Article
- ERK inhibition sensitizes CZ415-induced anti-osteosarcoma activityOncotarget · 2017Article
- microRNA-455 targets cullin 3 to activate Nrf2 signaling and protect human osteoblasts from hydrogen peroxide.Oncotarget · 2017Article
- Tumor-specific hepatic stellate cells (tHSCs) induces DIgR2 expression in dendritic cells to inhibit T cells.Oncotarget · 2017Article
- Article
- Ulk1 over-expression in human gastric cancer is correlated with patients' T classification and cancer relapse.Oncotarget · 2017Article
- AMPKα phosphatase Ppm1E upregulation in human gastric cancer is required for cell proliferation.Oncotarget · 2017Article
- Inhibiting DNA-PKBiochemical and biophysical research communications · 2017Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant osteosarcoma (OS) is still a deadly disease for many affected patients. The search for the novel anti-OS agent is extremely urgent and important. Our previous study has proposed that salinomycin is a novel anti-OS agent. Here we characterized DNA-dependent protein kinase catalytic subunit (DNA-PKcs) as a primary salinomycin resistance factor in OS cells. DNA-PKcs inhibitors (NU7026, NU7441 and LY294002) or DNA-PKcs shRNA knockdown dramatically potentiated salinomycin-induced death and apoptosis of OS cells (U2OS and MG-63 lines). Further, forced-expression of microRNA-101 ("miR-101") downregulated DNA-PKcs and augmented salinomycin's cytotoxicity against OS cells. Reversely, over-expression of DNA-PKcs in OS cells inhibited salinomycin's lethality. For the mechanism study, we show that DNA-PKcs is required for salinomycin-induced pro-survival autophagy activation. DNA-PKcs inhibition (by NU7441), shRNA knockdown or miR-101 expression inhibited salinomycin-induced Beclin-1 expression and autophagy induction. Meanwhile, knockdown of Beclin-1 by shRNA significantly sensitized salinomycin-induced OS cell lethality. In vivo, salinomycin administration suppressed U2OS xenograft tumor growth in severe combined immuno-deficient (SCID) mice, and its anti-tumor activity was dramatically potentiated with co-administration of the DNA-PKcs inhibitor NU7026. Together, these results suggest that DNA-PKcs could be a primary resistance factor of salinomycin in OS cells. DNA-PKcs inhibition or silence may thus significantly increase salinomycin's sensitivity in OS cells.
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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.