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小豆蔻明通过激活 P38 和 JNK 信号通路抑制人骨肉瘤细胞的生长。

Cardamonin inhibits the growth of human osteosarcoma cells through activating P38 and JNK signaling pathway.

机构信息

School of Laboratory Medicine, Chongqing Medical University, Chongqing, China.

Department of Orthopedics, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

出版信息

Biomed Pharmacother. 2021 Feb;134:111155. doi: 10.1016/j.biopha.2020.111155. Epub 2020 Dec 25.

Abstract

Osteosarcoma (OS) is the most common type of bone malignant tumors. Clinical commonly used therapeutic drugs of OS treatment are prone to toxic and side effects, so it is very urgent to develop new drugs with low toxicity and low side effects. As a Chinese herbal medicine, Cardamonin (CAR) (CHO) has inhibitory effects in various tumors. In the present study, we investigated the effects of CAR on OS cells in vitro and in vivo. We found that CAR inhibited cell proliferation, reduced migration, decreased invasion, and induced G2 / M arrest of OS cells. Notably, we demonstrated that CAR had no obvious effect on proliferation and apoptosis of normal cells. Besides, CAR repressed tumor growth of OS cells in xenograft mouse model. Mechanically, we found that CAR increased the phosphorylation level of P38 and JNK. In summary, our research validates that CAR may inhibit the proliferation, migration, and invasion of OS and promote apoptosis possibly by activating P38 and JNK Mitogen-activated protein kinase (MAPK) signaling pathway.

摘要

骨肉瘤(OS)是最常见的骨恶性肿瘤类型。临床常用的 OS 治疗治疗药物容易产生毒性和副作用,因此开发低毒性、低副作用的新药非常迫切。作为一种中草药,小豆蔻明(CAR)(CHO)在各种肿瘤中具有抑制作用。在本研究中,我们研究了 CAR 在体外和体内对 OS 细胞的作用。我们发现 CAR 抑制细胞增殖,减少迁移,降低侵袭,并诱导 OS 细胞 G2/M 期阻滞。值得注意的是,我们证明 CAR 对正常细胞的增殖和凋亡没有明显影响。此外,CAR 抑制异种移植小鼠模型中 OS 细胞的肿瘤生长。在机制上,我们发现 CAR 增加了 P38 和 JNK 的磷酸化水平。总之,我们的研究证实,CAR 可能通过激活 P38 和 JNK 丝裂原活化蛋白激酶(MAPK)信号通路来抑制 OS 的增殖、迁移和侵袭,并促进细胞凋亡。

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