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Protein BTG1 (B-cell translocation gene 1 protein)


Effects of hydrogen peroxide, doxorubicin and ultraviolet irradiation on senescence of human dental pulp stem cells.

The objective of this study was to evaluate the ability of three distinct agents on the induction of senescence in human dental pulp stem cells (DPSCs). DPSCs from three separate donors were treated with H O , doxorubicin and ultraviolet (UV) irradiation. The response of the cells to the three agents was assayed by specific staining for SA-βGal, RT-qPCR and flow cytometry. The results showed that incubation with 100 μM H O and 20 nM Doxorubicin for seven days led to senescence in all donors' cells equally. Interestingly, UV irradiation for just one minute was sufficient to induce senescence in the cells. The SA-βGal positive senescent cells were arrested in G phase and their S phase was significantly reduced as analyzed by flow cytometry. Significant increment in p21 and BTG1 expression and decrement in CCND1 expression also confirmed the cells have been arrested and get senescent via p53-p21 pathway. All three agents successfully triggered senescence in the cells. There was no significant difference in the capacity of the three donor's cells for senescence. To avoid premature senescence in stem cell in vitro, it is recommended to avoid unnecessary exposure of the cell to fluorescent and UV light. Moreover, to prevent ROS production, we recommend using a separate incubator with low oxygen content for cell culture, if possible.

MeSH Terms

  • Cells, Cultured
  • Cellular Senescence
  • Dental Pulp
  • Doxorubicin
  • Humans
  • Hydrogen Peroxide
  • Stem Cells
  • Ultraviolet Rays


  • Cell cycle
  • ROS
  • Stress induced senescence
  • Ultraviolet irradiation
  • p21

Tumor cell escape from therapy-induced senescence.

H460 non-small cell lung, HCT116 colon and 4T1 breast tumor cell lines induced into senescence by exposure to either etoposide or doxorubicin were able to recover proliferative capacity both in mass culture and when enriched for the senescence-like phenotype by flow cytometry (based on β-galactosidase staining and cell size, and a senescence-associated reporter, BTG1-RFP). Recovery was further established using both real-time microscopy and High-Speed Live-Cell Interferometry (HSLCI) and was shown to be accompanied by the attenuation of the Senescence-Associated Secretory Phenotype (SASP). Cells enriched for the senescence-like phenotype were also capable of forming tumors when implanted in both immunodeficient and immunocompetent mice. As chemotherapy-induced senescence has been identified in patient tumors, our results suggest that certain senescence-like phenotypes may not reflect a terminal state of growth arrest, as cells that recover with self-renewal capacity may ultimately contribute to disease recurrence.

MeSH Terms

  • Animals
  • Antineoplastic Agents
  • Cell Line, Tumor
  • Cell Proliferation
  • Cellular Senescence
  • HCT116 Cells
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, SCID
  • Tumor Burden
  • Xenograft Model Antitumor Assays


  • Cancer
  • Doxorubicin
  • Etoposide
  • Senescence
  • Tumor dormancy