ArticleBMC cancer2016
Long-lasting reduction in clonogenic potential of colorectal cancer cells by sequential treatments with 5-azanucleosides and topoisomerase inhibitors.
Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- AKAP2 is required for assembly of cytoskeletal signaling complexes that promote growth and metastasis of triple-negative breast cancer.The Journal of biological chemistry · 2026Article
- Hydroxychavicol in Combination with 5-Fluorouracil Induced Apoptosis by Inhibiting Purine Metabolism in HT-29 and DLD-1 Cell Lines.Chinese journal of integrative medicine · 2026Article
- Aromatic sulphonamides of aziridine-2-carboxylic acid derivatives as novel PDIA1 and PDIA3 inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- The Contrasting Delayed Effects of Transient Exposure of Colorectal Cancer Cells to Decitabine or Azacitidine.Cancers · 2022Article
- Sphingomyelin nanosystems loaded with uroguanylin and etoposide for treating metastatic colorectal cancer.Scientific reports · 2021Article
- Targeting Epigenetic Modifiers Can Reduce the Clonogenic Capacities of Sézary Cells.Frontiers in oncology · 2021Article
- Article
- Hypermethylation and decreased expression of TMEM240 are potential early-onset biomarkers for colorectal cancer detection, poor prognosis, and early recurrence prediction.Clinical epigenetics · 2020Article
- Hypermethylation ofOncotarget · 2017Article
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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
backgroundThe currently approved therapies fail in a substantial number of colorectal cancer (CRC) patients due to the molecular heterogeneity of CRC, hence new efficient drug combinations are urgently needed. Emerging data indicate that 5-azanucleosides are able to sensitize cancer cells to the standard chemotherapeutic agents and contribute to overcoming intrinsic or acquired chemoresistance.
methodsCRC cells with different genetic backgrounds (HCT116, DLD-1, HT-29) were sequentially treated with 5-azanucleosides and topoisomerase inhibitors. The combined effects of these two drug classes on cell viability, apoptosis, signaling pathways, and colony formation were investigated.
resultsHere, we demonstrate that pretreatment with DNA demethylating agents, 5-aza-2'-deoxycytidine and 5-azacytidine, sensitizes CRC cells to topoisomerase inhibitors (irinotecan, etoposide, doxorubicin, mitoxantrone), reducing cell viability and clonogenicity and increasing programmed cell death more effectively than individual compounds at the same or even higher concentrations. 5-Azanucleosides did not cause considerable immediate toxic effects as evaluated by analysis of cell viability, apoptosis, DNA damage (γH2A.X), and endoplasmic reticulum (ER) stress (CHOP). However, 5-azanucleosides exerted long-lasting effects, reducing cell viability, changing cell morphology, and affecting phosphoinositide 3-kinase (PI3-kinase)/Akt signaling pathway. We found that a single exposure to 5-azanucleosides is sufficient to induce long-lasting sensitization to topoisomerase inhibitors. The combinatorial, but not separate, treatment with low doses of 5-aza-2'-deoxycytidine (0.1 μM) and etoposide (0.5 μM) caused a long-lasting (almost 70 days) reduction in clonogenic/replating ability of DLD-1 cells.
conclusionsThese results suggest that sequential treatments with DNA demethylating agents and topoisomerase inhibitors may exert clinically relevant anticancer effects.
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