[Therapeutic mechanism of aqueous extract of Chang root for pancreatic cancer: the active components, therapeutic targets and pathways].

Y Huang, L Qin, S Guan, Y Guang, Y Wei, A Cao, D Li, G Wei, Q Su
Author Information
  1. Y Huang: College of Health Science, Guangdong Pharmaceutical University, Guangzhou 510006, China.
  2. L Qin: College of Health Science, Guangdong Pharmaceutical University, Guangzhou 510006, China.
  3. S Guan: School of Pharmaceutical Sciences, Sun Yatsen University, Guangzhou 510060, China.
  4. Y Guang: School of Pharmaceutical Sciences, Sun Yatsen University, Guangzhou 510060, China.
  5. Y Wei: School of Pharmaceutical Sciences, Sun Yatsen University, Guangzhou 510060, China.
  6. A Cao: School of Pharmaceutical Sciences, Sun Yatsen University, Guangzhou 510060, China.
  7. D Li: Guangxi Key Laboratory of Traditional Chinese Medicine Quality Standards, Guangxi Institute of Chinese Medicine and Pharmaceutical Science, Nanning 530022, China.
  8. G Wei: Guangxi Key Laboratory of Traditional Chinese Medicine Quality Standards, Guangxi Institute of Chinese Medicine and Pharmaceutical Science, Nanning 530022, China.
  9. Q Su: College of Health Science, Guangdong Pharmaceutical University, Guangzhou 510006, China.

Abstract

OBJECTIVE: To explore the key targets and signaling pathways in the therapeutic mechanism of Chang (SC) root against pancreatic cancer network pharmacology and molecular docking studies and cell experiments.
METHODS: The targets of SC and pancreatic cancer were predicted using the network pharmacological database, the protein-protein interaction network was constructed, and pathways, functional enrichment and molecular docking analyses were performed. CCK-8 assay was used to test the inhibitory effect of the aqueous extract of SC root on 8 cancer cell lines, and its effects on invasion, migration, proliferation, and apoptosis of pancreatic cancer cells were evaluated. Western blotting was performed to verify the results of network pharmacology analysis.
RESULTS: We identified a total of 18 active components in SC, which regulated 21 potential key targets in pancreatic cancer. GO and KEGG pathway enrichment analyses showed that these targets were involved mainly in the biological processes including protein phosphorylation, signal transduction, and apoptosis and participated in cancer signaling and PI3K-Akt signaling pathways. Among the 8 cancer cell lines, The aqueous extract of SC root produced the most obvious inhibitory effect in pancreatic cancer cells, and significantly inhibited the invasion, migration, and proliferation and promoted apoptosis of pancreatic cancer Panc-1 cells ( < 0.05). Western blotting confirmed that SC significantly inhibited the phosphorylation levels of PI3K and AKT in Panc-1 cells ( < 0.001).
CONCLUSION: The therapeutic effect of SC root against pancreatic cancer effects is mediated by its multiple components that act on different targets and pathways including the PI3K-Akt pathway.

Keywords

References

  1. JAMA. 2021 Sep 7;326(9):851-862 [PMID: 34547082]
  2. Neoplasia. 2015 Feb;17(2):175-82 [PMID: 25748236]
  3. Mol Cancer. 2020 May 4;19(1):82 [PMID: 32366257]
  4. J Ethnopharmacol. 2023 Jun 12;309:116306 [PMID: 36858276]
  5. Med Sci Monit. 2021 Jan 09;27:e924778 [PMID: 33419959]
  6. Pharmacol Ther. 2019 Sep;201:202-213 [PMID: 31158393]
  7. Phytomedicine. 2019 May;58:152762 [PMID: 31005717]
  8. Curr Biol. 2011 May 10;21(9):779-86 [PMID: 21514161]
  9. Nat Prod Res. 2021 Mar;35(6):960-966 [PMID: 31135220]
  10. Chin Herb Med. 2022 Sep 01;14(4):535-542 [PMID: 36405063]
  11. Crit Rev Oncol Hematol. 2022 Aug;176:103749 [PMID: 35728737]
  12. J Integr Med. 2017 Jul;15(4):282-287 [PMID: 28659232]
  13. Mol Cancer. 2017 Jan 31;16(1):23 [PMID: 28137273]
  14. Kidney Blood Press Res. 2018;43(1):220-233 [PMID: 29490297]
  15. Cancer Res. 2023 Sep 15;83(18):3077-3094 [PMID: 37363990]
  16. Cytokine Growth Factor Rev. 2018 Feb;39:46-61 [PMID: 29373197]
  17. Molecules. 2019 Nov 13;24(22): [PMID: 31766221]
  18. Cell. 2011 Mar 4;144(5):646-74 [PMID: 21376230]
  19. J Clin Oncol. 2010 Mar 1;28(7):1254-61 [PMID: 20100961]
  20. Biomed Pharmacother. 2020 Mar;123:109616 [PMID: 31881485]
  21. BMC Cancer. 2021 Apr 12;21(1):396 [PMID: 33845796]
  22. Semin Cancer Biol. 2022 May;80:58-72 [PMID: 32070764]
  23. Cancer Sci. 2010 Nov;101(11):2351-60 [PMID: 20726858]
  24. Gastroenterology. 2021 Feb;160(3):744-754 [PMID: 33058868]
  25. Cell Death Dis. 2023 Aug 4;14(8):497 [PMID: 37542052]
  26. Saudi J Gastroenterol. 2019 Jan-Feb;25(1):3-13 [PMID: 30588953]
  27. PLoS One. 2013 Dec 31;8(12):e83922 [PMID: 24391846]
  28. CA Cancer J Clin. 2016 Jan-Feb;66(1):7-30 [PMID: 26742998]
  29. J Ethnopharmacol. 2023 Aug 10;312:116454 [PMID: 37059246]
  30. Pharmacol Res. 2020 Nov;161:105130 [PMID: 32818653]

MeSH Term

Humans
Pancreatic Neoplasms
Cell Line, Tumor
Signal Transduction
Molecular Docking Simulation
Apoptosis
Cell Proliferation
Cell Movement
Plant Roots
Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Drugs, Chinese Herbal
Network Pharmacology
Plant Extracts
Protein Interaction Maps

Chemicals

Phosphatidylinositol 3-Kinases
Proto-Oncogene Proteins c-akt
Drugs, Chinese Herbal
Plant Extracts

Word Cloud

Created with Highcharts 10.0.0cancerpancreaticSCtargetsrootnetworkpathwayscellssignalingtherapeuticChangpharmacologymoleculardockingcelleffectaqueousextractapoptosiscomponentspathwaykeymechanismenrichmentanalysesperformedinhibitory8lineseffectsinvasionmigrationproliferationWesternblottinganalysisactiveincludingphosphorylationPI3K-AktsignificantlyinhibitedPanc-1<0OBJECTIVE:explorestudiesexperimentsMETHODS:predictedusingpharmacologicaldatabaseprotein-proteininteractionconstructedfunctionalCCK-8assayusedtestevaluatedverifyresultsRESULTS:identifiedtotal18regulated21potentialGOKEGGshowedinvolvedmainlybiologicalprocessesproteinsignaltransductionparticipatedAmongproducedobviouspromoted05confirmedlevelsPI3KAKT001CONCLUSION:mediatedmultipleactdifferent[Therapeuticcancer:pathways]Semiliquidambarcathayensis

Similar Articles

Cited By