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<p>Cyanobacteria have long attracted scientific interest through their potential application in the development of new therapeutic approaches, particularly those related to the treatment of cancer. In this study, the antiproliferative effects of <i>Nostoc commune</i> extract (NOS) and the cyanobacterial compound scytonemin (SCY) were evaluated against a variety of in vitro cancer models, including cervix, colon, breast, lung, and leukemia cell lines, using resazurin assays. Both of the studied compounds were found to have inhibited metabolic activity in a dose-dependent manner, with IC<sub>50</sub> values ranging from 60.5 to 462.0&#xa0;µM for SCY and 157.0 to 740.3&#xa0;µM for NOS. SCY displayed higher levels of inhibitory activity than NOS against all of the tested cancer models, but was particularly effective against HL-60 and Jurkat leukemia cells, with IC<sub>50</sub> values recorded as 60.5&#xa0;µM and 88.2&#xa0;µM, respectively. However in contrast, the two compounds exhibited significantly lower levels of inhibition against non-cancerous MCF-10A and BJ-5ta cells. Flow cytometry studies of leukemia cells treated with SCY revealed that the compound had effectively inhibited cell proliferation over prolonged periods; HL-60 cells displayed G1 phase arrest which lasted for 48&#xa0;h, while an accumulated G0/G1 sub-population was detected in Jurkat cells, as indicator of apoptosis. Further analysis of cells treated with SCY observed reduced levels of Rb protein and an increase in p21 expression in both HL-60 and Jurkat cell lines. Apoptotic markers such as phosphatidylserine externalization were observed, and mitochondrial dysfunction characterized by the dissipation of mitochondrial membrane potential was also detected. SCY activated the mitochondrial apoptotic pathway, inducing cytochrome <i>c</i> release and subsequent caspase-9, -3, and -7 activation. Finally, PARP cleavage, a typical marker of apoptosis, was identified in both leukemia cell lines following treatment with SCY. The findings suggest that SCY induces apoptosis in leukemia cells through the activation of the mitochondrial pathway, highlighting its potential for development as a future anti-cancer agent.</p>

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Nostoc commune-derived scytonemin induced mitochondrial cell death in leukemia models

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月17日

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  • Simona Zilakova,
  • Martina Gavurova,
  • Dominika Sebova,
  • Michal Goga,
  • Martin Backor,
  • Viktoria Medvecova,
  • Dajana Kecsey,
  • Martin Kello

摘要

Cyanobacteria have long attracted scientific interest through their potential application in the development of new therapeutic approaches, particularly those related to the treatment of cancer. In this study, the antiproliferative effects of Nostoc commune extract (NOS) and the cyanobacterial compound scytonemin (SCY) were evaluated against a variety of in vitro cancer models, including cervix, colon, breast, lung, and leukemia cell lines, using resazurin assays. Both of the studied compounds were found to have inhibited metabolic activity in a dose-dependent manner, with IC50 values ranging from 60.5 to 462.0 µM for SCY and 157.0 to 740.3 µM for NOS. SCY displayed higher levels of inhibitory activity than NOS against all of the tested cancer models, but was particularly effective against HL-60 and Jurkat leukemia cells, with IC50 values recorded as 60.5 µM and 88.2 µM, respectively. However in contrast, the two compounds exhibited significantly lower levels of inhibition against non-cancerous MCF-10A and BJ-5ta cells. Flow cytometry studies of leukemia cells treated with SCY revealed that the compound had effectively inhibited cell proliferation over prolonged periods; HL-60 cells displayed G1 phase arrest which lasted for 48 h, while an accumulated G0/G1 sub-population was detected in Jurkat cells, as indicator of apoptosis. Further analysis of cells treated with SCY observed reduced levels of Rb protein and an increase in p21 expression in both HL-60 and Jurkat cell lines. Apoptotic markers such as phosphatidylserine externalization were observed, and mitochondrial dysfunction characterized by the dissipation of mitochondrial membrane potential was also detected. SCY activated the mitochondrial apoptotic pathway, inducing cytochrome c release and subsequent caspase-9, -3, and -7 activation. Finally, PARP cleavage, a typical marker of apoptosis, was identified in both leukemia cell lines following treatment with SCY. The findings suggest that SCY induces apoptosis in leukemia cells through the activation of the mitochondrial pathway, highlighting its potential for development as a future anti-cancer agent.