ArticleBiochimica et biophysica acta2016
Nitric oxide inhibits topoisomerase II activity and induces resistance to topoisomerase II-poisons in human tumor cells.
Article in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Ferroptosis Inducers Erastin and RSL3 Enhance Adriamycin and Topotecan Sensitivity in ABCB1/ABCG2-Expressing Tumor Cells.International journal of molecular sciences · 2025Article
- The evolution of S-nitrosylation detection methodology and the role of protein S-nitrosylation in various cancers.Cancer cell international · 2024Review
- Mechanisms of Cell Death Induced by Erastin in Human Ovarian Tumor Cells.International journal of molecular sciences · 2024Article
- Soluble guanylate cyclase signalling mediates etoposide resistance in progressing small cell lung cancer.Nature communications · 2021Article
- Article
- Design, Synthesis and Anti-Tumor Activity of Novel Benzimidazole-Chalcone Hybrids as Non-Intercalative Topoisomerase II Catalytic Inhibitors.Molecules (Basel, Switzerland) · 2020Article
- Small Nucleolar RNAs Determine Resistance to Doxorubicin in Human Osteosarcoma.International journal of molecular sciences · 2020Article
- Role of Oxygen and Nitrogen Radicals in the Mechanism of Anticancer Drug Cytotoxicity.Journal of cancer science & therapy · 2020Article
- Reversal of drug resistance by JS-K and nitric oxide in ABCB1- and ABCG2-expressing multi-drug resistant human tumor cells.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2019Article
- In vitro investigating of anticancer activity of new 7-MEOTA-tacrine heterodimers.Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Nitric oxide reverses drug resistance by inhibiting ATPase activity of p-glycoprotein in human multi-drug resistant cancer cells.Biochimica et biophysica acta. General subjects · 2018Article
- Article
- Nitric oxide inhibits ATPase activity and induces resistance to topoisomerase II-poisons in human MCF-7 breast tumor cells.Biochemistry and biophysics reports · 2017Article
- Review
- Apoferritin as an ubiquitous nanocarrier with excellent shelf life.International journal of nanomedicine · 2017Article
- Nitric oxide: Friend or Foe in Cancer Chemotherapy and Drug Resistance: A Perspective.Journal of cancer science & therapy · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEtoposide and doxorubicin, topoisomerase II poisons, are important drugs for the treatment of tumors in the clinic. Topoisomerases contain several free sulfhydryl groups which are important for their activity and are also potential targets for nitric oxide (NO)-induced nitrosation. NO, a physiological signaling molecule nitrosates many cellular proteins, causing altered protein and cellular functions.
methodsHere, we have evaluated the roles of NO/NO-derived species in the activity/stability of topo II both in vitro and in human tumor cells, and in the cytotoxicity of topo II-poisons, etoposide and doxorubicin.
resultsTreatment of purified topo IIα with propylamine propylamine nonoate (PPNO), an NO donor, resulted in inhibition of both the catalytic and relaxation activity in vitro, and decreased etoposide-dependent cleavable complex formation in both human HT-29 colon and MCF-7 breast cancer cells. PPNO treatment also induced significant nitrosation of topo IIα protein in these human tumor cells. These events, taken together, caused a significant resistance to etoposide in both cell lines. However, PPNO had no effect on doxorubicin-induced cleavable complex formation, or doxorubicin cytotoxicity in these cell lines.
conclusionInhibition of topo II function by NO/NO-derived species induces significant resistance to etoposide, without affecting doxorubicin cytotoxicity in human tumor cells. GENERAL SIGNIFICANCE: As tumors express inducible nitric oxide synthase and generate significant amounts of NO, modulation of topo II functions by NO/NO-derived species could render tumors resistant to certain topo II-poisons in the clinic.
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