The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Berbamine, a novel nuclear factor κB inhibitor, inhibits growth and induces apoptosis in human myeloma cells
Open accessAbstract
Aim We sought to investigate the effect of berbamine on the growth of human multiple myeloma cell line KM3 and elucidate the mechanism of its action.Methods MTT assay was used to determine the inhibitory effect of berbamine alone or combined with chemotherapeutic drugs. Flow cytometry was performed to characterize cell cycle profile in response to berbamine treatment. Western blot was used to measure the protein levels of p65, IkappaB Kinase alpha (IKKalpha), TNFAIP3 (A20), IkappaBalpha, p-IkappaBalpha, cyclinD1, Bcl-2, BAX, Bcl-x(L), Bid, and survivin.Results Berbamine inhibits the proliferation of KM3 cells in a dose- and time-dependent manner. Combination of berbamine with dexamethasone (Dex), doxorubicin (Dox) or arsenic trioxide (ATO) resulted in enhanced inhibition of cell growth. Flow cytometric analysis revealed that KM3 cells were arrested at G(1) phase and apoptotic cells increased from 0.54% to 51.83% for 36 h. Morphological changes of cells undergoing apoptosis were observed under light microscope. Berbamine treatment led to increased expression of A20, down-regulation of IKKalpha, p-IkappaBalpha, and followed by inhibition of p65 nuclear localization. As a result, NF-kappaB downstream targets such as cyclinD1, Bcl-x(L), Bid and survivin were down-regulated.Conclusion Berbamine inhibits the growth of KM3 cells by inducing G(1) arrest as well as apoptosis. Berbamine blocks NF-kappaB signaling pathway through up-regulating A20, down-regulating IKKalpha, p-IkappaBalpha, and then inhibiting p65 nuclear translocation, and resulting in decreased expression of the downstream targets of NF-kappaB. Our results suggest that berbamine is a novel inhibitor of NF-kappaB activity with remarkable anti-myeloma efficacy.
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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 [635]
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 [635]
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 [635]
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Metadata
- Authors
- Liang, Y., Xu, R.-Z., Zhang, L., & Zhao, X.-Y.
- Affiliations
- Second Affiliated Hospital of Zhejiang University (CN)
- ORCID
- Zhang, Lei
- Venue
- Acta Pharmacologica Sinica
- Published
- 2009-12
- Volume
- 30
- Issue
- 12
- Pages
- 1659-1665
- ISSN
- 0253-9756 (ISSN-L)
- 1671-4083
- 1745-7254
- PMC
- PMC4007498
- OpenAlex
- W1976105081
- Cited by
- 61
- References
- 19
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 4 · 2023: 6 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 5 · 2014: 3 · 2013: 5 · 2012: 5
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Pharmacologica Sinica (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Health Sciences › Medicine › Pharmacology (medical) › Berberine and alkaloids research
- Keywords
- berbamine, multiple myeloma, NF-κB signaling, apoptosis, G1 cell cycle arrest, A20, IκBα, IKKα, p65 nuclear translocation, cyclin D1, Bcl-2 family proteins, survivin, dexamethasone, doxorubicin, arsenic trioxide, combination chemotherapy
- MeSH terms
- Tumor Necrosis Factor alpha-Induced Protein 3, Arsenic Trioxide, Anti-Inflammatory Agents, Non-Steroidal, Antineoplastic Agents, Arsenicals, Cell Nucleus, Dexamethasone, DNA-Binding Proteins, Doxorubicin, Humans, Multiple Myeloma, Nuclear Proteins, Oxides, Plasma Cells, Signal Transduction, G1 Phase, NF-kappa B, Apoptosis, Benzylisoquinolines, Cell Line, Tumor, Intracellular Signaling Peptides and Proteins, Cell Proliferation, I-kappa B Kinase
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