Induction of folate receptor type β in a bone marrow engraftment model of acute myelogenous leukemia

Blaser, Bradley W.; Gonit, Mesfin; Qi, Huiling; Shatnawi, Aymen; Guimond, Martin; Lee, R J; Ratnam, Manohar

doi:10.1038/sj.leu.2404786

Cited by 8 publications

(4 citation statements)

References 11 publications

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“…FR-β is expressed in approximately 70% of the cases of acute AML blast cells and is frequently co-expressed with CD34 (Pan et al, 2002), a common marker used to enriched populations of human hematopoietic stem cells (HSCs) and progenitors. FR-β is also expressed in bone marrow mononuclear cells of human AML engrafted NOD/SCID mice (Blaser et al, 2007), suggesting that FR-β is expressed in the AML progenitor cells and/or the AML stem cells. In addition, the expression of FR-β can be specifically upregulated by all-trans -retinoic acid (ATRA) in FR-β (+) KG-1 AML cells, MV4-11 AML cells, and primary AML cells (Pan et al, 2002; Blaser et al, 2007; Wang et al, 2000; Qi and Ratnam, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…FR-β is also expressed in bone marrow mononuclear cells of human AML engrafted NOD/SCID mice (Blaser et al, 2007), suggesting that FR-β is expressed in the AML progenitor cells and/or the AML stem cells. In addition, the expression of FR-β can be specifically upregulated by all-trans -retinoic acid (ATRA) in FR-β (+) KG-1 AML cells, MV4-11 AML cells, and primary AML cells (Pan et al, 2002; Blaser et al, 2007; Wang et al, 2000; Qi and Ratnam, 2006). Moreover, enhanced cytotoxicity of FR-targeted liposomal doxorubicin relative to non-targeted control liposomes was further enhanced by selective FR-β upregulation using ATRA (Pan et al, 2002; Lu et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

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Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid

Piao

et al. 2010

International Journal of Pharmaceutics

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Our previous data demonstrated that folate receptor β (FR-β) targeted liposomal doxorubicin (FT-L-DOX) showed enhanced cytotoxicity relative to non-targeted liposomal doxorubicin (CON-L-DOX), and the effect was enhanced by selective FR-β upregulation by all-trans retinoic acid (ATRA) in AML blast cells. In this study, the enhanced cytotoxicity was investigated in the proliferating human AML clonogenic cells by combining FT-L-DOX with ATRA. Also, pharmacokinetic properties by pretreatment of ATRA were evaluated using FR-targeted liposomal calcein (FT-L-Calcein). Pharmacokinetic study showed that the area under the concentration curve (AUC) of FT-L-Calcein was decreased and total clearance was increased by pretreatment with ATRA. Meanwhile, the volume of distribution was significantly increased by pretreatment of ATRA. Moreover, calcein level in the liver, spleen and kidney was increased following intravenous administration of FT-L-Calcein by pretreatment of ATRA. In vitro cytotoxicity of FT-L-DOX was higher than that of CON-L-DOX and was increased by pretreatment with ATRA. Colony formation in AML cells was lower due to treatment with FT-L-DOX compared with CON-L-DOX and colony formation further decreased upon pretreatment with ATRA. Moreover, FT-L-DOX was more toxic to AML clonogenic cells than to AML blast cells. The results demonstrate that the efficiency of FR-mediated targeting of FT-L-DOX was preferentially enhanced by ATRA induced FR-β upregulation in AML clonogenic cells.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid

Piao

et al. 2010

International Journal of Pharmaceutics

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“…HL60 cells are common human AML cells. Earlier studies reveal that folate receptor-β (FR-β) was overexpressed in promyelocytic leukemia [30][31][32]. Most investigators find that FA can specifically combine with folate receptors (FR) that are overexpressed on the cancer cell cytomembrane but are rarely expressed in normal blood cells [33][34][35].…”

Section: Introductionmentioning

confidence: 99%

Semiconductor Quantum Dots (CdX, X = S, Te, Se) Modify Titanium Dioxide Nanoparticles for Photodynamic Inactivation of Leukemia HL60 Cancer Cells

Pan

Xiao

et al. 2021

Journal of Nanomaterials

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Titanium dioxide nanoparticles (TiO2-NPs) are highly efficient photosensitizers in traditional photodynamic therapy (PDT). The particle size of TiO2-NPs is small, only about 20 nm. However, the demands of ultraviolet light (UV) excitation feature shallow tissue penetration depth and may lead to severe tissue photon damage. Thus, in this research, TiO2-NPs are modified with semiconductor quantum dots (QDs) CdX (X = S, Te, Se) in various methods, such as ultrasonic, hydrothermal, sol-gel, aqueous phase, and hydrolysis precipitation. The transmission electron microscopy (TEM) images show that the size of CdSe-TiO2 is ranging from 6 to 14 nm. The ultraviolet-visible (UV-Vis) spectrum demonstrates that the CdX (X = S, Te, Se) modification can successfully extend the absorption range of TiO2-NPs into a different visible light region. CdSe QDs have the narrowest band gap compared with CdX (X = S, Te, Se) QDs. Visible light-activated CdSe-TiO2 nanocomposite shows the highest PDT inactivation efficiency toward HL60 cells compared with CdX-TiO2. The photogenerated carrier separation efficiency of CdSe-TiO2 nanocomposite is the highest shown in a fluorescence spectrum (FS). Furthermore, when conjugated with folic acid (FA), the prepared FA-CdX-TiO2 (X = S, Se) exhibits excellent cancer-targeting ability during PDT treatment. Optimum PDT efficiency of FA-CdSe-TiO2 indicates that photocatalytic and targeting ability is much higher than pure TiO2 and CdSe-TiO2. Our results provided a detailed investigation on the PDT performance of CdX (X = S, Te, Se) modified TiO2 and may act as a guide for further design of highly targeted performance visible-light response TiO2-NPs.

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“…It seems that, given the critical role of activated macrophages in autoimmune diseases and tumors, a therapeutic agent that targets these cells will have wide applications in the clinic. A substantial fraction of chronic myelogenous leukemia and AML cells also express FRβ [16,17]. …”

Section: Introductionmentioning

confidence: 99%

A folate receptor beta-specific human monoclonal antibody recognizes activated macrophage of rheumatoid patients and mediates antibody-dependent cell-mediated cytotoxicity

Yang¹,

Shen

Streaker

et al. 2011

Arthritis Res Ther

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IntroductionFolate receptor beta (FRβ) is only detectable in placenta and limited to some hematopoietic cells of myeloid lineage in healthy people. Studies have indicated that FRβ is over-expressed in activated macrophages in autoimmune diseases and some cancer cells. In this study we aimed to develop an FRβ-specific human monoclonal antibody (mAb) that could be used as a therapeutic agent to treat rheumatoid arthritis and other autoimmune diseases, as well as FRβ positive cancers.MethodsFunctional recombinant FRβ protein was produced in insect cells and used as antigen to isolate a mAb, m909, from a human naïve Fab phage display library. Binding of Fab and IgG1 m909 to FRβ was measured by ELISA, surface plasmon resonance, immune fluorescence staining, and flow cytometry. Antibody-dependent cell-mediated cytotoxicity (ADCC) was evaluated with FRβ positive CHO cells as target cells and isolated peripheral blood monocytes as effector cells in an in vitro assay.ResultsFab m909 bound with relatively high affinity (equilibrium dissociation constant 57 nM) to FRβ. The IgG1 m909 showed much higher (femtomolar) avidity as measured by ELISA, and it bound to FRβ positive cells in a dose-dependent manner, but not to parental FRβ negative cells. m909 did not compete with folate for the binding to FRβ on cells. m909 was not only able to select FRβ positive, activated macrophages from synovial fluid cells of arthritis patients as efficiently as folate, but also able to mediate ADCC in FRβ positive cells.ConclusionsUnlike folate-drug conjugates, m909 selectively binds to FRβ, does not recognize FRα, and has at least one effector function. m909 alone has potential to eliminate FRβ positive cells. Because m909 does not compete with folate for receptor binding, it can be used with folate-drug conjugates in a combination therapy. m909 can also be a valuable research reagent.

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Induction of folate receptor type β in a bone marrow engraftment model of acute myelogenous leukemia

Cited by 8 publications

References 11 publications

Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid

Targeting human clonogenic acute myelogenous leukemia cells via folate conjugated liposomes combined with receptor modulation by all-trans retinoic acid

Semiconductor Quantum Dots (CdX, X = S, Te, Se) Modify Titanium Dioxide Nanoparticles for Photodynamic Inactivation of Leukemia HL60 Cancer Cells

A folate receptor beta-specific human monoclonal antibody recognizes activated macrophage of rheumatoid patients and mediates antibody-dependent cell-mediated cytotoxicity

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