Copyright (c) 2023 Yichao Liang, Jun Li, Honglin Xu, Mingjie Pang, Changlei Hu, Xie Weng, Wei Xie
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.Cepharanthine suppresses proliferation and metastasis and enhances apoptosis by regulating JAK2/Stat3 pathway in hepatocellular carcinoma
Corresponding Author(s) : Wei Xie
Cellular and Molecular Biology,
Vol. 69 No. 14: Cancer molecular biology: Diagnosis and treatment
Abstract
Hepatocellular carcinoma (HCC) is a familiar malignant tumor, and cepharanthine (CEP) was proven to prevent the malignant activity of multiple cancer cells, including HCC. However, there are few reports on the regulatory role of CEP in HCC. After treatment with CEP or/and JAK2/Stat3 inhibitor (AG490), the associative functions were assessed by MTT, wound healing, Trans well, and Hochest33342-PI double staining in HCC cells. Then the levels of CDK4, MMP-9, Bcl-2, p-JAK2/JAK2, and p-Stat3/Stat3 were monitored via western blot. Besides, the HCC xenograft model was constructed to verify the effects of CEP on tumor growth and the JAK/Stat3 pathway. CEP could restrain proliferation and metastasis and facilitate apoptosis in HCC cells. CEP also reduced Bcl-2 (anti-apoptosis), CDK4 (proliferation), and MMP-9 (invasion) expressions, and inhibited JAK2 and Stat3 phosphorylation. Besides, CEP suppressed HCC progression by JAK2/Stat3 pathway. Moreover, CEP inhibited the growth of subcutaneous HCC xenografts and reduced p-JAK2 and p-Stat3 in tumor tissues. CEP could suppress HCC progression by attenuating the JAK2/Stat3 pathway, indicating that CEP might be a therapeutic drug for HCC patients.
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