Department of Traumatic Orthopedics, Renmin Hospital, Hubei University of Medicine, Shiyan, 442000, P.R. China.
Anticancer Agents Med Chem. 2023;23(14):1670-1677. doi: 10.2174/1871520623666230420081738.
Trillium tschonoskii Maxim (TTM) exerts antitumor effects on a variety of tumour cells. However, the antitumor mechanism of Diosgenin glucoside (DG) extracted from TTM is not clear.
This study aimed to investigate the anti-tumour effects of DG-induced osteosarcoma MG-63 cells and their molecular mechanism.
CCK-8 assay, HE staining, and flow cytometry were used to detect the effects of DG on the proliferation, apoptosis, and cell cycle of osteosarcoma cells. Wound healing and Transwell invasion assays were used to observe the effect of DG on the migration and invasion of osteosarcoma cells. The anti-tumour mechanism of DG on osteosarcoma cells was investigated by immunohistochemistry, Western blot, and RT-PCR.
DG significantly inhibited osteosarcoma cell activity and proliferation, promoted apoptosis and blocked the G2 phase of the cell cycle. Both wound healing and Transwell invasion assays showed that DG inhibited osteosarcoma cell migration and invasion. Immunohistochemical and western blot results showed that DG inhibited the activation of PI3K/AKT/mTOR. We found that DG also significantly downregulated the expression of S6K1 and eIF4F, which might be associated with the inhibition of protein synthesis.
DG may inhibit proliferation, migration, invasion, and cell cycle G2 phase arrest of osteosarcoma MG-63 cells and promote apoptosis through the PI3K/AKT/mTOR signalling pathway.
延龄草（Trillium tschonoskii Maxim）提取物中的薯蓣皂苷元（Diosgenin glucoside，DG）对多种肿瘤细胞均具有抗肿瘤作用。然而，从延龄草中提取的薯蓣皂苷元（Diosgenin glucoside，DG）的抗肿瘤机制尚不清楚。
本研究旨在探讨 DG 对骨肉瘤 MG-63 细胞的抗肿瘤作用及其分子机制。
采用 CCK-8 法、HE 染色和流式细胞术检测 DG 对骨肉瘤细胞增殖、凋亡和细胞周期的影响。采用划痕愈合实验和 Transwell 侵袭实验观察 DG 对骨肉瘤细胞迁移和侵袭的影响。采用免疫组化、Western blot 和 RT-PCR 技术探讨 DG 对骨肉瘤细胞的抗肿瘤机制。
DG 显著抑制骨肉瘤细胞活性和增殖，促进细胞凋亡并阻滞细胞周期于 G2 期。划痕愈合实验和 Transwell 侵袭实验结果表明，DG 抑制骨肉瘤细胞迁移和侵袭。免疫组化和 Western blot 结果显示，DG 抑制了 PI3K/AKT/mTOR 的激活。我们发现 DG 还显著下调了 S6K1 和 eIF4F 的表达，这可能与抑制蛋白质合成有关。
DG 可能通过 PI3K/AKT/mTOR 信号通路抑制骨肉瘤 MG-63 细胞的增殖、迁移、侵袭和 G2 期阻滞，促进细胞凋亡。
