ArticleOncotarget2017
Bafilomycin A1 triggers proliferative potential of senescent cancer cells in vitro and in NOD/SCID mice.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 61 citations in OpenAlex.
- Tumor cells escape from therapy-induced senescence: from molecular mechanisms to targeted intervention.Biology direct · 2026Review
- Can Cancer Cell Line In Vitro Radioembolization Model Help to Understand How Beta Radiation Affects Liver Tumor and Improve Treatment Results?International journal of molecular sciences · 2026Article
- Vacuolar-ATPase inhibitors are antimicrobial agents active against intracellular mycobacteria.Antimicrobial agents and chemotherapy · 2025Article
- Bafilomycin A1 induces colon cancer cell death through impairment of the endolysosome system dependent on iron.Scientific reports · 2025Article
- Cellular senescence in colorectal cancer: its occurrence, effect and therapy.Frontiers in oncology · 2025Review
- A prognostic model based on autophagy-and senescence-related genes for gastric cancer: implications for immunotherapy and personalized treatment.Frontiers in oncology · 2025Article
- Targeting autophagy promotes the antitumor effect of radiotherapy on cervical cancer cells.Cancer biology & therapy · 2024Article
- Angiogenesis is limited by LIC1-mediated lysosomal trafficking.Angiogenesis · 2024Article
- Therapy-induced senescence through the redox lens.Redox biology · 2024Review
- Cancer stem cells: advances in knowledge and implications for cancer therapy.Signal transduction and targeted therapy · 2024Review
- Article
- A Conversation with ChatGPT on Contentious Issues in Senescence and Cancer Research.Molecular pharmacology · 2024Article
- Therapy-induced senescence is finally escapable, what is next?Cell cycle (Georgetown, Tex.) · 2024Review
- Therapy-induced senescent tumor cells in cancer relapse.Journal of the National Cancer Center · 2023Review
- BLM helicase overexpressed in human gliomas contributes to diverse responses of human glioma cells to chemotherapy.Cell death discovery · 2023Article
- Review
- Insights into the role of senescence in tumor dormancy: mechanisms and applications.Cancer metastasis reviews · 2023Review
- High Hemin Concentration Induces Escape from Senescence of Normoxic and Hypoxic Colon Cancer Cells.Cancers · 2022Article
- Therapy-Induced Senescent/Polyploid Cancer Cells Undergo Atypical Divisions Associated with Altered Expression of Meiosis, Spermatogenesis and EMT Genes.International journal of molecular sciences · 2022Article
- Targeting tumor cell senescence and polyploidy as potential therapeutic strategies.Seminars in cancer biology · 2022Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anticancer therapies that induce DNA damage tend to trigger senescence in cancer cells, a process known as therapy-induced senescence (TIS). Such cells may undergo atypical divisions, thus contributing to tumor re-growth. Accumulation of senescent cancer cells reduces survival of patients after chemotherapy. As senescence interplays with autophagy, a dynamic recycling process, we sought to study whether inhibition of autophagy interferes with divisions of TIS cells. We exposed human colon cancer HCT116 cells to repeated cycles of a chemotherapeutic agent - doxorubicin (doxo) and demonstrated induction of hallmarks of TIS (e.g. growth arrest, hypertrophy, poliploidization and secretory phenotype) and certain properties of cancer stem cells (increased NANOG expression, percentages of CD24+ cells and side population). Colonies of small and highly proliferative progeny appeared shortly after drug removal. Treatment with bafilomycin A1 (BAF A1), an autophagy inhibitor, postponed short term in vitro cell re-population. It was associated with reduction in the number of diploid and increase in the number of poliploid cells. In a long term, a pulse of BAF A1 resulted in reactivation of autophagy in a subpopulation of HCT116 cells and increased proliferation. Accordingly, the senescent HCT116 cells treated with BAF A1 when injected into NOD/SCID mice formed tumors, in contrast to the controls.Our results suggest that senescent cancer cells that appear during therapy, can be considered as dormant cells that contribute to cancer re-growth, when chemotherapeutic treatment is stopped. These data unveil new mechanisms of TIS-related cancer maintenance and re-population, triggered by a single pulse of BAF A1 treatment.
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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.