Hydroxysafflor yellow A induces autophagy in human liver cancer cells by regulating Beclin 1 and ERK expression
Hydroxysafflor yellow A induces autophagy in human liver cancer cells by regulating Beclin 1 and ERK expression
复制标题
羟基红花黄A通过调节Beclin 1和ERK表达诱导人肝癌细胞自噬
DOI：
10.3892/etm.2020.8552
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发表时间：
2020-04-01
影响因子：
2.7
通讯作者：
Wei, Peng
中科院分区：
文献类型：
--
作者：
Chen, Ziwei;Liu, Li;Wei, Peng
羟基红花黄A （Hydroxysafflor yellow A， HSYA）是红花（Carthamus tinctorius）的一种水溶性成分，研究表明HSYA具有抗肿瘤作用。本研究探讨了HSYA对Hep-G2肝癌细胞株自噬的影响及其机制。用HSYA处理Hep-G2细胞，用MTT法测定细胞活力。Western blotting和免疫荧光法检测轻链3 II （LC3-II）和p62以及自噬调节因子Beclin 1和ERK1/2的表达。透射电镜观察自噬体的形成。测定了HSYA与自噬抑制剂氯喹（CQ）的联合作用。结果表明，Hep-G2细胞活力随HSYA浓度的增加而降低。与对照组相比，HYSA组LC3-II表达显著升高，p62水平显著降低。此外，在HYSA处理的Hep-G2细胞中，Beclin 1表达增加，磷酸化erk1 /2表达减少。CQ和HSYA治疗后，与HSYA组相比，Hep-G2细胞的活力显著增加。综上所述，HSYA通过促进Beclin 1的表达和抑制ERK的磷酸化来诱导肝癌细胞自噬。因此，HSYA可能是一种潜在的肝癌治疗剂。
Hydroxysafflor yellow A (HSYA) is a water-soluble component of the safflower (Carthamus tinctorius), and research has revealed that HSYA exhibits antitumor effects. In the present study, the effects of HSYA on the autophagy of a Hep-G2 liver cancer cell line, as well as the underlying mechanisms, were investigated. Hep-G2 cells were treated with HSYA and the viability of cells was measured using an MTT assay. Western blotting and immunofluorescence assays were performed to determine the expression of light chain 3 II (LC3-II) and p62, as well as the autophagy regulators Beclin 1 and ERK1/2. Transmission electron microscopy was performed to observe the formation of autophagosomes. The combined effects of HSYA and the autophagy inhibitor chloroquine (CQ) were also determined. The results revealed that the viability of Hep-G2 cells decreased with increasing concentrations of HSYA. Furthermore, LC3-II expression increased significantly and the level of p62 decreased significantly in the HYSA group compared with the control group. Additionally, an increase in Beclin 1 expression and a decrease in phosphorylated-ERK1/2 expression was observed in Hep-G2 cells treated with HYSA. Following treatment with CQ and HSYA, a significant increase in the viability of Hep-G2 cells was observed compared with the HSYA group. Collectively, the results indicated that HSYA induced autophagy by promoting the expression of Beclin 1 and inhibiting the phosphorylation of ERK in liver cancer cells. Therefore, HSYA may serve as a potential therapeutic agent for liver cancer.