Curcumin in combination with bortezomib synergistically induced apoptosis in human multiple myeloma U266 cells

  title={Curcumin in combination with bortezomib synergistically induced apoptosis in human multiple myeloma U266 cells},
  author={Juwon Park and Vasudevan Ayyappan and Eunkyung Bae and Chansu Lee and Byung-Su Kim and Byoung Kook Kim and Young-Yuil Lee and Kwang Sung Ahn and Sung-Soo Yoon},
  journal={Molecular Oncology},
Sensitizing human multiple myeloma cells to the proteasome inhibitor bortezomib by novel curcumin analogs
It is shown that the water-soluble analog of curcumin #12, but notCurcumin, in combination with bortezomib could enhance the proteasome-inhibitory effect in multiple myeloma cells.
Curcumin ameliorates the in vitro efficacy of carfilzomib in human multiple myeloma U266 cells targeting p53 and NF-κB pathways.
Curcumin Enhanced Busulfan-Induced Apoptosis through Downregulating the Expression of Survivin in Leukemia Stem-Like KG1a Cells
It is demonstrated that CUR could increase the sensitivity of leukemia stem-like KG1a cells to BUS by downregulating the expression of survivin, especially in combination group.
Gambogenic acid synergistically potentiates bortezomib-induced apoptosis in multiple myeloma
The data support that a synergistic antitumor activity exists between BTZ and GNA, and provide a rationale for successful utilization of dual BTZ or GNA in MM chemotherapy in the future.
Curcumin Enhances Cytotoxic Effects of Bortezomib in Human Multiple Myeloma H929 Cells: Potential Roles of NF-κB/JNK
Results suggested that curcumin might enhance the cytotoxicity of PS-341 by interacting with NF-κB, at least in part, through JNK mechanism.
Curcumin Synergistically Enhances the Cytotoxicity of Arsenic Trioxide in U266 Cells by Increasing Arsenic Uptake
Curcumin can enhance the killing effects of ATO on U266 by increasing the intracellular arsenic content, which may be related to the upregulation of AQP9 expression.
Curcumin and Its Analogue Induce Apoptosis in Leukemia Cells and Have Additive Effects with Bortezomib in Cellular and Xenograft Models
A novel Mannich-type curcumin derivative, C-150, holds a great promise as a future therapeutic agent in the treatment of leukemia alone or in combination, and was synthesized to improve potency.
Curcumin induces cell death of the main molecular myeloma subtypes, particularly the poor prognosis subgroups
It is shown that primary myeloma cells were also sensitive to curcumin, even those displaying del(17p), another poor prognosis factor, and the contribution of anti-apoptotic Bcl-2 family molecules in Curcumin response is unraveled.


Multiple Myeloma. Advances in disease biology: therapeutic implications.
The survival and proliferation of multiple myeloma cells are largely dependent on a supportive microenvironment, and clinical trials using monoclonal antibodies to block IL-6 or its receptors are underway, and interleukin-6 is known for its ability to support cell growth and prevent apoptosis.
Advances in disease biology: Therapeutic implications
The malignant clone and the bone-marrow environment.
Targeting Multiple Myeloma Cells and Their Bone Marrow Microenvironment
Several studies have established the biologic significance of cytokines in MM pathogenesis and delineated signaling cascades mediating their effects, providing the framework for related novel therapies targeting not only the MM cell, but also the bone marrow microenvironment.
Bortezomib: A valuable new antineoplastic strategy in multiple myeloma
Preliminary results of several phase I and II studies are also showing high antimyeloma activity of bortezomib alone or in combination with dexamethasone or cytotoxic agents such as doxorubicin, mephalan, or thalidomide in patients with newly diagnosed multiple myeloma.
The proteasome as a potential target for novel anticancer drugs and chemosensitizers.
  • K. Landis-Piwowar, V. Milacic, Q. Dou
  • Biology, Chemistry
    Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy
  • 2006
Unraveling the biology of multiple myeloma disease: cancer stem cells, acquired intracellular changes and interactions with the surrounding micro-environment.
The biology of multiple myeloma, a malignant bone marrow disorder consisting of monoclonal plasma cells accumulation, is described, stressing the origin of Myeloma cells, their acquired genetic changes and interactions with their bone marrow microenvironment.
The proteasome inhibitor PS-341 markedly enhances sensitivity of multiple myeloma tumor cells to chemotherapeutic agents.
  • Mark H Ma, Hank H. Yang, J. Berenson
  • Biology, Chemistry
    Clinical cancer research : an official journal of the American Association for Cancer Research
  • 2003
Results suggest that inhibition of NF-kappaB with PS-341 may overcome chemoresistance and allow doses of chemotherapeutic agents to be markedly reduced with antitumor effects without significant toxicity.
Adhesion of human myeloma-derived cell lines to bone marrow stromal cells stimulates interleukin-6 secretion.
The binding of myeloma cells to BMSCs was partially blocked with anti- beta 1 monoclonal antibody (MoAb), anti-beta 2 integrin MoAb, and excess RGD peptide, suggesting multiple mechanisms for the adhesion of myeeloma cell lines to B MSCs.
Curcumin (diferuloylmethane) down-regulates the constitutive activation of nuclear factor–κB and IκBα kinase in human multiple myeloma cells, leading to suppression of proliferation and induction of apoptosis
It is found that curcumin down-regulates NF-κB in human MM cells, leading to the suppression of proliferation and induction of apoptosis, thus providing the molecular basis for the treatment of MM patients with this pharmacologically safe agent.