The Water Extract of Juniperus communis L. Induces Cell Death and Sensitizes Cancer Cells to Cytostatic Drugs through p53 and PI3K/Akt Pathways

• Published in: International journal of molecular sciences Vol. 20; no. 9; p. 2054
• Main Authors: Raasmaja, Atso, Stenius, Ulla, Ghalali, Aram
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 26-04-2019; MDPI
• Subjects: 1-Phosphatidylinositol 3-kinase; A549 non-small lung cancer cells; Acetylation; Akt; AKT protein; Apoptosis; Cancer therapies; Cell death; Cytosol; Deacetylation; Dephosphorylation; Fruits; Gene expression; Juniperus communis; Juniperus communis L; Kinases; Liver cancer; Medicin och hälsovetenskap; Nuclear transport; p53; p53 Protein; Phenolic compounds; Phenols; Phosphorylation; Physiological effects; plant extract; Polyphenols; Proteins; Tumor suppressor genes; plant extract; Akt; Juniperus communis L; A549 non-small lung cancer cells; cell death; p53
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms20092054

Juniper (
L.) is a northern coniferous plant generally used as a spice and for nutritional purposes in foods and drinks. It was previously reported that juniper extract (JE) affects p53 activity, cellular stress, and gene expression induced cell death in human neuroblastoma cells. Therefore, the effects of juniper on p53 and Akt signaling was examined further in A549 lung, 22RV1 and DU145 prostate, and HepG2 liver cancer cells using Western blot, confocal microscopy, and MTT analysis. We found that juniper simultaneously decreased cell viability, activated the p53 pathway, and inactivated the PI3K/Akt pathway. The p53 activation was associated with increased nuclear p53 level. Akt was dephosphorylated, and its inactivation was associated with increased levels of PHLPP1 and PHLPP2 phosphatases. Parallel increases of PARP suggest that JE decreased cell viability by activating cell death. In adtion, JE potentiated the effects of gemcitabine and 5-fluorouracil anticancer drugs. Thus, JE can activate cell death in different cancer cell lines through p53 and Akt pathways.