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<p>Endoplasmic reticulum (ER) stress is the accumulation of misfolded or defective proteins in the ER. ER stress is capable of inducing both anti-apoptotic and pro-apoptotic cellular response, and at the same time plays an important role in metabolism and progression of many types of tumors. Current understanding of the role of ER stress in changing functional parameters of normal and tumor cells is lacking. This study investigated how ER stress inducers bortezomib, dithiothreitol, and tunicamycin influence proliferation, cell cycle, and changes in ploidy of normal and tumor cells of epidermal origin HaCaT and A431 in vitro following incubation with the agent as well as after its removal from the culture medium. Bortezomib caused a cell cycle arrest in the G2 phase in HaCaT&#xa0;cells, as well as polyploidization in both cell lines. Dithiothreitol induced apoptosis in HaCaT&#xa0;cells. Tunicamycin caused a decrease in proliferative index, cell cycle arrest, as well as apoptosis and necrosis in the A431 cells. In conclusion, induction of ER stress by different mechanisms has different effects on normal and tumor cells and can lead to both polyploidization and, presumably, cell differentiation or senescence.</p>

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ER stress affects proliferation and induces polyploidization of cultured human HaCaT and A431 cells

  • 期刊论文

  • 发表日期：

    2026年4月13日

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  • Ilia I. Zakharov,
  • Polina A. Veselova,
  • Margarita A. Savitskaya,
  • Elena A. Smirnova,
  • Galina E. Onishchenko

摘要

Endoplasmic reticulum (ER) stress is the accumulation of misfolded or defective proteins in the ER. ER stress is capable of inducing both anti-apoptotic and pro-apoptotic cellular response, and at the same time plays an important role in metabolism and progression of many types of tumors. Current understanding of the role of ER stress in changing functional parameters of normal and tumor cells is lacking. This study investigated how ER stress inducers bortezomib, dithiothreitol, and tunicamycin influence proliferation, cell cycle, and changes in ploidy of normal and tumor cells of epidermal origin HaCaT and A431 in vitro following incubation with the agent as well as after its removal from the culture medium. Bortezomib caused a cell cycle arrest in the G2 phase in HaCaT cells, as well as polyploidization in both cell lines. Dithiothreitol induced apoptosis in HaCaT cells. Tunicamycin caused a decrease in proliferative index, cell cycle arrest, as well as apoptosis and necrosis in the A431 cells. In conclusion, induction of ER stress by different mechanisms has different effects on normal and tumor cells and can lead to both polyploidization and, presumably, cell differentiation or senescence.