DNA fragmentation, apoptosis and cell cycle arrest induced by sodium arsenite in cultured murine Sertoli cells: prevention by curcumin

Jellyfish venom is a rich source of bioactive proteins and peptides with various biological activities including antioxidant, antimicrobial and antitumor effects. However, the anti-proliferative activity of the crude extract of Rhopilema nomadica jellyfish venom has not been examined yet. The present study aimed at the investigation of the in vitro effect of R. nomadica venom on liver cancer cells (HepG2), breast cancer cells (MDA-MB231), human normal fibroblast (HFB4), and human normal lung cells (WI-38) proliferation by using MTT assay. The apoptotic cell death in HepG2 cells was investigated using Annexin V-FITC/PI double staining-based flow cytometry analysis, western blot analysis, and DNA fragmentation assays. R. nomadica venom displayed significant dose-dependent cytotoxicity on HepG2 cells after 48 h of treatment with IC50 value of 50 μg/mL and higher toxicity (3:5-fold change) against MDA-MB231, HFB4, and WI-38 cells. R. nomadica venom showed a prominent increase of apoptosis as revealed by cell cycle arrest at G2/M phase, upregulation of p53, BAX, and caspase-3 proteins, and the down-regulation of anti-apoptotic Bcl-2 protein and DNA fragmentation. These findings suggest that R. nomadica venom induces apoptosis in hepatocellular carcinoma cells. To the best of the authors’ knowledge, this is the first scientific evidence demonstrating the induction of apoptosis and cell cycle arrest of R. nomadica jellyfish venom.

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Balsamin induces apoptosis in breast cancer cells via DNA fragmentation and cell cycle arrest

Molecular and Cellular Biochemistry ◽

10.1007/s11010-017-3009-x ◽

2017 ◽

Vol 432 (1-2) ◽

pp. 189-198 ◽

Cited By ~ 13

Author(s):

Parminder K. Ajji ◽

Marley J. Binder ◽

Ken Walder ◽

Munish Puri

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cell Cycle Arrest ◽

Cancer Cells ◽

Dna Fragmentation ◽

Breast Cancer Cells ◽

Cycle Arrest

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Loss of splicing factor ASF/SF2 induces G2 cell cycle arrest and apoptosis, but inhibits internucleosomal DNA fragmentation

Genes & Development ◽

10.1101/gad.1359305 ◽

2005 ◽

Vol 19 (22) ◽

pp. 2705-2714 ◽

Cited By ~ 98

Author(s):

X. Li

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Dna Fragmentation ◽

Splicing Factor ◽

Cycle Arrest ◽

G2 Cell Cycle Arrest

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Novel molecular discovery of promising amidine-based thiazole analogues as potent dual Matrix Metalloproteinase-2 and 9 inhibitors: Anticancer activity data with prominent cell cycle arrest and DNA fragmentation analysis effects

Bioorganic Chemistry ◽

10.1016/j.bioorg.2020.103992 ◽

2020 ◽

Vol 101 ◽

pp. 103992 ◽

Cited By ~ 2

Author(s):

Abdelsattar M. Omar ◽

Jürgen Bajorath ◽

Saleh Ihmaid ◽

Hany M. Mohamed ◽

Ahmed M. El-Agrody ◽

...

Keyword(s):

Cell Cycle ◽

Matrix Metalloproteinase ◽

Anticancer Activity ◽

Cell Cycle Arrest ◽

Dna Fragmentation ◽

Matrix Metalloproteinase 2 ◽

Activity Data ◽

Cycle Arrest

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The Effects of Autophagy and PI3K/AKT/m-TOR Signaling Pathway on the Cell-Cycle Arrest of Rats Primary Sertoli Cells Induced by Zearalenone

Toxins ◽

10.3390/toxins10100398 ◽

2018 ◽

Vol 10 (10) ◽

pp. 398 ◽

Cited By ~ 14

Author(s):

Bing-jie Wang ◽

Wang-long Zheng ◽

Nan-nan Feng ◽

Tao Wang ◽

Hui Zou ◽

...

Keyword(s):

Cell Cycle ◽

Cell Cycle Arrest ◽

Signaling Pathway ◽

Germ Cells ◽

Sertoli Cells ◽

Cell Cycle Distribution ◽

High Concentration ◽

Tor Signaling ◽

Cycle Arrest

A high concentration of Zearalenone (ZEA) will perturb the differentiation of germ cells, and induce a death of germ cells, but the toxic mechanism and molecular mechanism remain unclear. The Sertoli cells (SCs) play an irreplaceable role in spermatogenesis. In order to explore the potential mechanism of ZEA male reproductive toxicity, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins and autophagy-related pathway the PI3K/Akt/mTOR signaling in primary cultured rats SCs, and the effects of autophagy and PI3K/AKT/m TOR signaling pathway on the SCs cell-cycle arrest induced by ZEA treated with the autophagy promoter RAPA, autophagy inhibitor CQ, and the PI3K inhibitor LY294002, respectively. The data revealed that ZEA could inhibit the proliferation of SCs by arresting the cell cycle in the G2/M phase and trigger the autophagy via inhibiting the PI3K/Akt/m TOR signaling pathway. Promoting or inhibiting the level of autophagy could either augment or reverse the arrest of cell cycle. And it was regulated by PI3K/Akt/m TOR signaling pathway. Taken together, this study provides evidence that autophagy and PI3K/Akt/m TOR signaling pathway are involved in regulating rats primary SCs cell-cycle arrest due to ZEA in vitro. To some extent, ZEA-induced autophagy plays a protective role in this process.

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