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| Main Authors: | , , , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
Marine biotechnology (New York, N.Y.)
2026
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| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41493638/ |
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Table of Contents:
- Investigating the Effects of Sea Anemone (Stichodactyla haddoni) Toxin on Potassium and Sodium Channel Gene Expression and Cell Death Mechanisms in A549 Cells. Abdollahian, Media Bardeei, Latifeh Karimzadeh Nabiuni, Mohammad Pourfallah, Mostafa Animals Mice Sea Anemones NIH 3T3 Cells A549 Cells Humans Reactive Oxygen Species Cnidarian Venoms Sodium Channels Cell Survival YAP-Signaling Proteins Antineoplastic Agents Marine Toxins Cell Cycle Apoptosis Lung cancer is one of the leading causes of death worldwide, and chemotherapy, despite being one of the main methods of treating this type of cancer, has several adverse side effects. Therefore, recent pharmaceutical research has focused on finding alternative treatments with natural sources and fewer side effects. Toxins from the Cnidaria phylum have shown potential since they contain bioactive proteins and peptides with anticancer properties. This study investigated the effects of Stichodactyla haddoni (S. haddoni) Sea Anemone Extract (SAE), a species from this phylum, on A549 lung cancer cells and NIH3T3 (embryonic mouse fibroblast cells). SAE was prepared, and the cells, A549 and NIH3T3, were treated with a series of concentrations (50-300 µg/mL) from the extract. The cell survival rate was measured after 24, 48, and 72 h using an MTT assay. The cell cycle distribution and intracellular reactive oxygen species (ROS) production were measured using flow cytometry. The expression level of KCNC4, SCN9A, and YAP1 genes was reported using real-time PCR. The IC50 values of the SAE in the A549 cell line were 50, 67, and 70 µg/mL after 24, 48, and 72 h, respectively. SAE exhibited dose-dependent cytotoxicity in both A549 lung cancer cells and NIH/3T3 fibroblasts; however, a lower IC₅₀ value was observed in A549 cells (50 µg/mL) compared with NIH/3T3 cells (67 µg/mL) after 24 h, suggesting preferential toxicity toward cancer cells. With an increase in the concentration of SAE from 25 to 75 µg/mL, the percentage of apoptotic cells increased. In addition, the 50 µg/mL concentration of SAE significantly increased intracellular ROS and decreased the percentage of S-phase cells in the cell cycle after 24 h. KCNC4, SCN9A, and YAP1 expression levels were lower compared to the control group. S. haddoni SAE is a potential natural anticancer agent that affects KCNC4 and SCN9A in a concentration-dependent and time-independent manner.