RT Journal Article SR Electronic T1 Astragaloside IV Induces Apoptosis, G1-Phase Arrest and Inhibits Anti-apoptotic Signaling in Hepatocellular Carcinoma JF In Vivo JO In Vivo FD International Institute of Anticancer Research SP 631 OP 638 DO 10.21873/invivo.11817 VO 34 IS 2 A1 CHUN-MIN SU A1 HSIAO-CHIA WANG A1 FEI-TING HSU A1 CHUN-HUI LU A1 CHIEN-KAI LAI A1 JING-GUNG CHUNG A1 YU-CHENG KUO YR 2020 UL http://iv.iiarjournals.org/content/34/2/631.abstract AB 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 G1 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.