ArticleBMC cancer2013
N-benzyladriamycin-14-valerate (AD 198) exhibits potent anti-tumor activity on TRAF3-deficient mouse B lymphoma and human multiple myeloma.
Article in BMC cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Upregulated Expression of the IL-9 Receptor on TRAF3-Deficient B Lymphocytes Confers Ig Isotype Switching Responsiveness to IL-9 in the Presence of Antigen Receptor Engagement and IL-4.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- The adaptor protein TRAF3 is an immune checkpoint that inhibits myeloid-derived suppressor cell expansion.Frontiers in immunology · 2023Article
- The intrinsically disordered CARDs-Helicase linker in RIG-I is a molecular gate for RNA proofreading.The EMBO journal · 2022Article
- Mitochondrial Fission Factor Is a Novel Interacting Protein of the Critical B Cell Survival Regulator TRAF3 in B Lymphocytes.Frontiers in immunology · 2021Article
- Pivarubicin Is More Effective Than Doxorubicin Against Triple-Negative Breast Cancer In Vivo.Oncology research · 2020Article
- Elevated Choline Kinase α-Mediated Choline Metabolism Supports the Prolonged Survival of TRAF3-Deficient B Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Mutations of p53 decrease sensitivity to the anthracycline treatments in bladder cancer cells.Oncotarget · 2018Article
- Formulation, Development, and In Vitro Evaluation of a CD22 Targeted Liposomal System Containing a Non-Cardiotoxic Anthracycline for B Cell Malignancies.Pharmaceutics · 2018Article
- Identification of the Multifaceted Chemopreventive Activity of Curcumin Against the Carcinogenic Potential of the Food Additive, KBrO3.Current pharmaceutical design · 2018Article
- Signaling mechanisms of bortezomib in TRAF3-deficient mouse B lymphoma and human multiple myeloma cells.Leukemia research · 2016Article
- Article
- Targeting TRAF3 Downstream Signaling Pathways in B cell Neoplasms.Journal of cancer science & therapy · 2015Article
- Myeloid cell TRAF3 regulates immune responses and inhibits inflammation and tumor development in mice.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- A novel derivative of doxorubicin, AD198, inhibits canine transitional cell carcinoma and osteosarcoma cells in vitro.Drug design, development and therapy · 2015Article
- Spatiotemporal pattern of TRAF3 expression after rat spinal cord injury.Journal of molecular histology · 2014Article
- Mutated in colorectal cancer (MCC) is a novel oncogene in B lymphocytes.Journal of hematology & oncology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTRAF3, a new tumor suppressor identified in human non-Hodgkin lymphoma (NHL) and multiple myeloma (MM), induces PKCδ nuclear translocation in B cells. The present study aimed to evaluate the therapeutic potential of two PKCδ activators, N-Benzyladriamycin-14-valerate (AD 198) and ingenol-3-angelate (PEP005), on NHL and MM.
methodsIn vitro anti-tumor activities of AD 198 and PEP005 were determined using TRAF3-/- mouse B lymphoma and human patient-derived MM cell lines as model systems. In vivo therapeutic effects of AD 198 were assessed using NOD SCID mice transplanted with TRAF3-/- mouse B lymphoma cells. Biochemical studies were performed to investigate signaling mechanisms induced by AD 198 or PEP005, including subcellular translocation of PKCδ.
resultsWe found that AD 198 exhibited potent in vitro and in vivo anti-tumor activity on TRAF3-/- tumor B cells, while PEP005 displayed contradictory anti- or pro-tumor activities on different cell lines. Detailed mechanistic investigation revealed that AD 198 did not affect PKCδ nuclear translocation, but strikingly suppressed c-Myc expression and inhibited the phosphorylation of ERK, p38 and JNK in TRAF3-/- tumor B cells. In contrast, PEP005 activated multiple signaling pathways in these cells, including PKCδ, PKCα, PKCε, NF-κB1, ERK, JNK, and Akt. Additionally, AD198 also potently inhibited the proliferation/survival and suppressed c-Myc expression in TRAF3-sufficient mouse and human B lymphoma cell lines. Furthermore, we found that reconstitution of c-Myc expression conferred partial resistance to the anti-proliferative/apoptosis-inducing effects of AD198 in human MM cells.
conclusionsAD 198 and PEP005 have differential effects on malignant B cells through distinct biochemical mechanisms. Our findings uncovered a novel, PKCδ-independent mechanism of the anti-tumor effects of AD 198, and suggest that AD 198 has therapeutic potential for the treatment of NHL and MM involving TRAF3 inactivation or c-Myc up-regulation.
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