ArticleDoklady. Biochemistry and biophysics2020
Prostate Cancer Growth Inhibition by 1-(3,5-Dimethylphenyl)-6-methyl-1H-pyrazolo[4,3-c]pyridin-4(5H)-one via Down-regulation of Phosphorylation PI3K/AKT and STA3/JAK2.
Article in Doklady. Biochemistry and biophysics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Cellular and Molecular Evidence of the Synergistic Antitumour Effects of Hydroxytyrosol and Metformin in Prostate Cancer.International journal of molecular sciences · 2025Article
- Comparative Cytotoxic Activity of Hydroxytyrosol and Its Semisynthetic Lipophilic Derivatives in Prostate Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
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3 authors at 1 institution in 1 country.
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Abstract
In the present study, 1-(3,5-dimethylphenyl)-6-methyl-1H-pyrazolo[4,3-c]pyridin-4 (5H)-one (DPMPP) was investigated as an antiproliferative agent for prostate cancer cells and the mechanism of its action was studied. Cell lines 22Rv1 and SGC‑7901 were used as in vitro models of prostate cancer. The DPMPP treatment inhibited proliferation of 22Rv1 and SGC‑7901 cells in dose-depended manner. The viability of 22Rv1 and SGC‑7901 cells was reduced to 21 and 19%, respectively after treatment with 32 µM DPMPP. In DPMPP treated (16 µM) 22Rv1 and SGC‑7901 cells apoptosis increased to 62.78 and 68.51%, respectively. Moreover, DPMPP treatment caused cell cycle arrest in S phase and inhibition of PI3K/AKT activation. In the same time ROS production showed elevation and MMP (Matrix MetalloProteinase) decreased in the cells. Apparently DPMPP induces cytotoxicity through induction of oxidative response and apoptosis in prostate cancer cells in vitro. The PI3K/Akt/ERK phosphorylation was inhibited, while p21 and p53, death receptor, expression was promoted by DPMPP treatment. Therefore, DPMPP has a potential to be used as a therapeutic agent for treatment of prostate cancer.
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