Open Access

Effect of 23‑hydroxybetulinic acid on lung adenocarcinoma and its mechanism of action

  • Authors:
    • Boyu Tan
    • Xiaoxu Lan
    • Yifan Zhang
    • Pai Liu
    • Qiyao Jin
    • Zhiqiang Wang
    • Zhidong Liang
    • Wei Song
    • Ye Xuan
    • Yunxiao Sun
    • Youjie Li
  • View Affiliations

  • Published online on: March 28, 2024     https://doi.org/10.3892/etm.2024.12527
  • Article Number: 239
  • Copyright: © Tan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The present study aimed to investigate the effect and mechanism of Pulsatilla compounds on lung adenocarcinoma. The representative drug chosen was the compound 23‑HBA. GeneCards, Swiss target prediction, DisGeNET and TCMSP were used to screen out related genes, and MTT and flow cytometry assays were used to verify the inhibitory effect of Pulsatilla compounds on the proliferation of lung adenocarcinoma cells. Subsequently, the optimal target, peroxisome proliferator‑activated receptor (PPAR)‑γ, was selected using bioinformatics analysis, and its properties of low expression in lung adenocarcinoma cells and its role as a tumor suppressor gene were verified by western blot assay. The pathways related to immunity and inflammation, vascular function, cell proliferation, differentiation, development and apoptosis with the highest degree of enrichment and the mechanisms were explored through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses. Finally, the clinical prognosis in terms of the survival rate of patients in whom the drug is acting on the target was analyzed using the GEPIA database. The results indicated that Pulsatilla compounds can inhibit the proliferation of lung adenocarcinoma cells by blocking the cell cycle at the G1 phase. Subsequently, the related PPAR‑γ gene was verified as a tumor suppressor gene. Further analysis demonstrated that this finding was related to the PPAR signaling pathway and mitochondrial reactive oxygen species (ROS) production. Finally, the clinical prognosis was found to be improved, as the survival rate of patients was increased. In conclusion, Pulsatilla compounds were indicated to inhibit the viability and proliferation of lung adenocarcinoma H1299 cells, and the mechanism of action was related to PPAR‑γ, the PPAR signaling pathway and mitochondrial ROS. The present study provides novel insight to further explore the treatment of lung adenocarcinoma.
View Figures
View References

Related Articles

Journal Cover

June-2024
Volume 27 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Tan B, Lan X, Zhang Y, Liu P, Jin Q, Wang Z, Liang Z, Song W, Xuan Y, Sun Y, Sun Y, et al: Effect of 23‑hydroxybetulinic acid on lung adenocarcinoma and its mechanism of action. Exp Ther Med 27: 239, 2024
APA
Tan, B., Lan, X., Zhang, Y., Liu, P., Jin, Q., Wang, Z. ... Li, Y. (2024). Effect of 23‑hydroxybetulinic acid on lung adenocarcinoma and its mechanism of action. Experimental and Therapeutic Medicine, 27, 239. https://doi.org/10.3892/etm.2024.12527
MLA
Tan, B., Lan, X., Zhang, Y., Liu, P., Jin, Q., Wang, Z., Liang, Z., Song, W., Xuan, Y., Sun, Y., Li, Y."Effect of 23‑hydroxybetulinic acid on lung adenocarcinoma and its mechanism of action". Experimental and Therapeutic Medicine 27.6 (2024): 239.
Chicago
Tan, B., Lan, X., Zhang, Y., Liu, P., Jin, Q., Wang, Z., Liang, Z., Song, W., Xuan, Y., Sun, Y., Li, Y."Effect of 23‑hydroxybetulinic acid on lung adenocarcinoma and its mechanism of action". Experimental and Therapeutic Medicine 27, no. 6 (2024): 239. https://doi.org/10.3892/etm.2024.12527