Astragaloside IV Induces Apoptosis, G1-Phase Arrest and Inhibits Anti-apoptotic Signaling in Hepatocellular Carcinoma

Background/Aim: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver and the third leading cause of cancer death worldwide. Although multiple chemotherapies options are available for HCC, chemo-induced toxicity is inevitable during clinical treatment. Therefore, identifying possible a...

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Veröffentlicht in:In vivo (Athens) 2020-03, Vol.34 (2), p.631-638
Hauptverfasser: SU, CHUN-MIN, WANG, HSIAO-CHIA, HSU, FEI-TING, LU, CHUN-HUI, LAI, CHIEN-KAI, CHUNG, JING-GUNG, KUO, YU-CHENG
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Sprache:eng
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Zusammenfassung:Background/Aim: Hepatocellular carcinoma (HCC) is a primary malignancy of the liver and the third leading cause of cancer death worldwide. Although multiple chemotherapies options are available for HCC, chemo-induced toxicity is inevitable during clinical treatment. Therefore, identifying possible adjuvant agents with both liver-protective and antitumor effects is critical. Herbal medicines have chemopreventive and anti-HCC effect, such as Juzen taiho-to and Sho-saiko-to. Astragaloside IV is a compound extracted from the Chinese medical herb Astragalus membranaceus (Fisch.) Bge. with liver protection potential. However, whether astragaloside IV may also possess tumor-inhibitory capability and its underlying mechanism is remaining unknown. Materials and Methods: Viability analysis, cell-cycle analysis, apoptosis analysis, western blotting analysis and invasion trans-well assay were performed to identify tumor-inhibitory potential of astragaloside IV on HCC cells (SK-Hep1 and Hep3B cells). Results: We found that astragaloside IV may induce cytotoxicity and extrinsic/intrinsic apoptosis effect, but also trigger G 1 arrest in HCC cells. The expression of anti-apoptotic proteins of HCC were all reduced by astragaloside IV. Additionally, astragaloside IV also suppressed HCC cell invasion ability. Conclusion: Astragaloside IV effectively suppressed HCC cell proliferation, invasion and anti-apoptosis in vitro.
ISSN:0258-851X
1791-7549
DOI:10.21873/invivo.11817