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Peer-reviewedCC BY 4.0PLOS One

Anticancer activity of asiatic acid in cisplatin-resistant human neuroblastoma SH-SY5Y and its unaffected effect on human neural stem cells

  • Apisada Jiso1
  • Laphatrada Yurasakpong2
  • Amarin Thongsuk3
  • Tarinee Chodchavanchai4
  • Nisarat Ruangsawasdi5
  • Permphan Dharmasaroja6
  • Anupong Thongklam Songsaad
  • Taweesak Tangrodchanapong
6 affiliations
  1. 1Department of Pharmaceutical Sciences, Faculty of Pharmacy, Chiang Mai University, Chiang Mai, Thailand
  2. 2Chakri Naruebodindra Medical Institute, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Samut Prakan, Thailand
  3. 3Department of Anatomy, Faculty of Science, Mahidol University, Bangkok, Thailand
  4. 4Department of Pharmacology, Faculty of Dentistry, Mahidol University, Bangkok, Thailand
  5. 5Department of Anatomy, Faculty of Dentistry, Mahidol University, Bangkok, Thailand
  6. 6School of Radiological Technology, Faculty of Health Science Technology, Chulabhorn Royal Academy, Bangkok, Thailand
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Abstract

Objective: To investigate the anticancer effects of asiatic acid (AA) and asiaticoside (AS) in cisplatin (Cis)-resistant neuroblastoma SH-SY5Y and neural stem cells derived from human stem cells from apical papilla (NSCs-hSCAPs). Methods: An MTT cell viability assay was performed to determine Cis toxicity and assess the cytotoxic effect of AA or AS on Cis-treated SH-SY5Y and the effect on NSCs-hSCAPs. Subsequently, the combination index (CI) was calculated to observe occurring interactions between the compound and Cis. For mechanistic exploration, flow cytometry using annexin V and PI staining and a caspase-3 activity assay were done to quantify apoptotic cell death. qRT-PCR was used to measure apoptotic and antioxidant mRNA levels. Additionally, the protein levels were analyzed by using the Western blot technique. Finally, to illustrate the putative interactions between the compound and its target, molecular docking was trialled. Results: MTT results revealed that AS did not affect both cells. However, 20 µM AA in combination with 2.5 µM Cis could significantly reduce SH-SY5Y cell viability with a CI value of 0.41, indicating their synergistic effect. Moreover, the effective concentration of AA did not affect Cis-treated NSCs-hSCAPs, suggesting its low toxicity. Considering SH-SY5Y, AA alone or its combination dramatically increased % apoptotic cells, which showed a minimal increment in Cis alone. Importantly, the combination treatment significantly increased caspase-3 activity. Mechanistically, BAX levels were elevated, whereas BCL2, SOD-1, and HO-1 levels were downregulated by AA alone or in combination. These results were also consistent with Western blot analysis. Interestingly, an inhibition of GSK3β was observed in the combination treatment, suggesting that these outcomes may be related.The molecular docking illustrated that AA interacted with GSK3β and BCL-2 through multiple residues, indicating their potential binding interactions. Conclusion: AA and Cis treatment suppressed SH-SY5Y cell viability by enhancing apoptosis, reducing antioxidant gene expression, and potentially inhibiting GSK3β.

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Cite

BibTeXRIS
BibTeX
@article{jiso2026anticancer,
  title = {{Anticancer activity of asiatic acid in cisplatin-resistant human neuroblastoma SH-SY5Y and its unaffected effect on human neural stem cells}},
  author = {Apisada Jiso and Laphatrada Yurasakpong and Amarin Thongsuk and Tarinee Chodchavanchai and Nisarat Ruangsawasdi and Permphan Dharmasaroja and Anupong Thongklam Songsaad and Taweesak Tangrodchanapong},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0358134},
  url = {https://doi.org/10.1371/journal.pone.0358134},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Anticancer activity of asiatic acid in cisplatin-resistant human neuroblastoma SH-SY5Y and its unaffected effect on human neural stem cells
AU  - Apisada Jiso
AU  - Laphatrada Yurasakpong
AU  - Amarin Thongsuk
AU  - Tarinee Chodchavanchai
AU  - Nisarat Ruangsawasdi
AU  - Permphan Dharmasaroja
AU  - Anupong Thongklam Songsaad
AU  - Taweesak Tangrodchanapong
PY  - 2026
DA  - 2026/09/15
JO  - PLOS One
DO  - 10.1371/journal.pone.0358134
UR  - https://doi.org/10.1371/journal.pone.0358134
AB  - Objective: To investigate the anticancer effects of asiatic acid (AA) and asiaticoside (AS) in cisplatin (Cis)-resistant neuroblastoma SH-SY5Y and neural stem cells derived from human stem cells from apical papilla (NSCs-hSCAPs). Methods: An MTT cell viability assay was performed to determine Cis toxicity and assess the cytotoxic effect of AA or AS on Cis-treated SH-SY5Y and the effect on NSCs-hSCAPs. Subsequently, the combination index (CI) was calculated to observe occurring interactions between the compound and Cis. For mechanistic exploration, flow cytometry using annexin V and PI staining and a caspase-3 activity assay were done to quantify apoptotic cell death. qRT-PCR was used to measure apoptotic and antioxidant mRNA levels. Additionally, the protein levels were analyzed by using the Western blot technique. Finally, to illustrate the putative interactions between the compound and its target, molecular docking was trialled. Results: MTT results revealed that AS did not affect both cells. However, 20 µM AA in combination with 2.5 µM Cis could significantly reduce SH-SY5Y cell viability with a CI value of 0.41, indicating their synergistic effect. Moreover, the effective concentration of AA did not affect Cis-treated NSCs-hSCAPs, suggesting its low toxicity. Considering SH-SY5Y, AA alone or its combination dramatically increased % apoptotic cells, which showed a minimal increment in Cis alone. Importantly, the combination treatment significantly increased caspase-3 activity. Mechanistically, BAX levels were elevated, whereas BCL2, SOD-1, and HO-1 levels were downregulated by AA alone or in combination. These results were also consistent with Western blot analysis. Interestingly, an inhibition of GSK3β was observed in the combination treatment, suggesting that these outcomes may be related.The molecular docking illustrated that AA interacted with GSK3β and BCL-2 through multiple residues, indicating their potential binding interactions. Conclusion: AA and Cis treatment suppressed SH-SY5Y cell viability by enhancing apoptosis, reducing antioxidant gene expression, and potentially inhibiting GSK3β.
SN  - 1932-6203
ER  -