4.5 Article

Apigenin, a flavonoid constituent derived from P. villosa, inhibits hepatocellular carcinoma cell growth by CyclinD1/CDK4 regulation via p38 MAPK-p21 signaling

Journal

PATHOLOGY RESEARCH AND PRACTICE
Volume 216, Issue 1, Pages -

Publisher

ELSEVIER GMBH
DOI: 10.1016/j.prp.2019.152701

Keywords

P. villosa juss; Apigenin; Cell cycle; CyclinD1/CDK4 regulation; p38 MAPK-p21 signaling

Categories

Funding

  1. Beijing Excellent Talent Project [2015400685627G240]
  2. National Natural Science Foundation of China [81303211, 81500439]
  3. China Postdoctoral Science Foundation [2013M540301]
  4. Beijing Municipal Administration of Hospitals' Youth Program [QML20161801, QML20171801]

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Hepatocellular carcinoma (HCC) is a leading cause of cancer mortality worldwide. Apigenin was widely used in HCC treatment; however, the detailed mechanisms have not been clarified. We isolated, characterized, and identified Apigenin from the P. villosa plant using ethanol-extracted, semi-preparative HPLC and NMR. MTT was used to detect the cytotoxicity of Apigenin in HepG2, SMMC-7721 and Huh-7 cell lines. The cell cycle changes of Apigenin on HepG2 using flow cytometry and the key molecules of cell cycle regulation by RT-qPCR and Western blot. Apigenin was ethanol-extracted and semi-preparative HPLC was used for isolation and purification. The compounds were identified and the results showed Apigenin was one of the bioactive compounds. Apigenin exhibited relatively high cytotoxicity in HepG2, SMMC-7721, and Huh-7. Cell cycle analysis showed that Apigenin could induce G1 arrest in HepG2 in a dose-dependent manner. CyclinD1 was up-regulated and CDK4 was down-regulated upon Apigenin treatment, which indicated that Apigenin could block cell cycle progression at the G1 phase though the regulation of CDK4 and CyclinD1 expression. In conclusion, the present findings might provide new insights about the implication of Apigenin and P. villosa in cancer therapy.

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