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Berbamine Inhibits the Growth of Liver Cancer Cells and Cancer-Initiating Cells by Targeting Ca2+/Calmodulin-Dependent Protein Kinase II
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Abstract
Liver cancer is the third leading cause of cancer deaths worldwide but no effective treatment toward liver cancer is available so far. Therefore, there is an unmet medical need to identify novel therapies to efficiently treat liver cancer and improve the prognosis of this disease. Here, we report that berbamine and one of its derivatives, bbd24, potently suppressed liver cancer cell proliferation and induced cancer cell death by targeting Ca2+/calmodulin-dependent protein kinase II (CAMKII). Furthermore, berbamine inhibited the in vivo tumorigenicity of liver cancer cells in NOD/SCID mice and downregulated the self-renewal abilities of liver cancer–initiating cells. Chemical inhibition or short hairpin RNA–mediated knockdown of CAMKII recapitulated the effects of berbamine, whereas overexpression of CAMKII promoted cancer cell proliferation and increased the resistance of liver cancer cells to berbamine treatments. Western blot analyses of human liver cancer specimens showed that CAMKII was hyperphosphorylated in liver tumors compared with the paired peritumor tissues, which supports a role of CAMKII in promoting human liver cancer progression and the potential clinical use of berbamine for liver cancer therapies. Our data suggest that berbamine and its derivatives are promising agents to suppress liver cancer growth by targeting CAMKII. Mol Cancer Ther; 12(10); 2067–77. ©2013 AACR.
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CAMKIIγ, encoded by CAMK2G, was proven to be an essential target to inhibit T cell lymphoma by destabilizing c-Myc.
“Later, Ca2+/calmodulin-dependent protein kinase II γ (CAMKIIγ), which was encoded by CAMK2G, was proven to be an essential target to inhibit T cell lymphoma by destabilizing c-Myc.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [636]
High-throughput siRNA screening in 2012 by Grandori's group identified a network of genes required for survival of c-Myc overexpressing cells, among which CAMK2G was screened out and further verified as the most potential gene in such networks.
“High-throughput siRNA screening in 2012 Grandori’s group identified a network of genes required for survival of c-Myc overexpressing cells, among which CAMK2G was screened out and further verified as the most potential gene in such networks.”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [636]
Inhibiting CAMKIIγ with its specific inhibitor berbamine suppressed development of T cell lymphoma and reduced tumor burden.
“Inhibiting CAMKIIγ with its specific inhibitor berbamine could suppress development of T cell lymphoma and reduce tumor burden.635,636”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [636]
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Metadata
- Authors
- Meng, Z., Li, T., Ma, X., Wang, X., Van Ness, C., Gan, Y., Zhou, H., Tang, J., Lou, G., Wang, Y., Wu, J., Yen, Y., Xu, R., & Huang, W.
- Affiliations
- City Of Hope National Medical Center (US)
- Authors' Affiliations: 1Irell & Manella Graduate School of Biological Sciences, Departments of 2Diabetes and Metabolic Diseases Research, 3Molecular Pharmacology, and 4Comparative Medicine, Beckman Research Institute, City of Hope National Medical Center, Duarte, California; 5Department of Biochemistry and Molecular Biology, Third Military Medical University, Chongqing; 6Department of Hematology (Key Laboratory of Cancer Prevention and Intervention, China National Ministry of Education), 7Cancer Institute, Second Affiliated Hospital, 8Department of Colorectal Surgery and Biomedical Research Center, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China
- Corresponding author
- Xu, Rongzhen
- Huang, Wendong
- ORCID
- Venue
- Molecular Cancer Therapeutics
- Published
- 2013-10-01
- Volume
- 12
- Issue
- 10
- Pages
- 2067-2077
- ISSN
- 1535-7163 (ISSN-L)
- 1538-8514
- PMC
- PMC3808882
- OpenAlex
- W2160088467
- Cited by
- 97
- References
- 39
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 9 · 2023: 8 · 2022: 10 · 2021: 11 · 2020: 8 · 2019: 2 · 2018: 8 · 2017: 10 · 2016: 5 · 2015: 4 · 2014: 3 · 2013: 2
- FWCI
- 2.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Cancer Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Hope Center for Neurological Disorders
- National Natural Science Foundation of China (81270601)
- National Cancer Institute (R01CA139158, P30CA033572)
- Topics
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Health Sciences › Medicine › Pharmacology (medical) › Berberine and alkaloids research
- Health Sciences › Medicine › Oncology › Cancer Cells and Metastasis
- Keywords
- berbamine, liver cancer, hepatocellular carcinoma, calcium/calmodulin-dependent protein kinase II, CaMKII, cancer stem cells, self-renewal, cell proliferation, apoptosis, tumor growth inhibition, CaMKII phosphorylation, drug resistance, natural product derivatives
- MeSH terms
- Animals, Humans, Liver Neoplasms, Gene Expression Regulation, Neoplastic, Apoptosis, Xenograft Model Antitumor Assays, Benzylisoquinolines, Cell Proliferation, Mice, Calcium-Calmodulin-Dependent Protein Kinase Type 2
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