HIV-1 protease inhibitor ritonavir potentiates the effect of 1,25-dihydroxyvitamin D3 to induce growth arrest and differentiation of human myeloid leukemia cells via down-regulation of CYP24

Ikezoe, Takayuki; Bandobashi, Kentaro; Yang, Ye; Takeuchi, Seisho; Sekiguchi, Nobuo; Sakai, Shuichi; Koeffler, H. Phillip; Taguchi, Hirokuni

doi:10.1016/j.leukres.2005.12.008

Cited by 23 publications

(12 citation statements)

References 22 publications

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“…These cells have also been used to screen methodologies or drugs that may inhibit HIV-1 infection or reduce transcriptional activation of the virus [117,[160][161][162][163][164][165][166][167][168][169][170][171][172][173]. These cell lines have also been used in studies of drug toxicity, permeability, and/or effects on cellular activation and differentiation to gain an understanding of what specific drugs might do to cells in the bone marrow [144,154,[174][175][176][177][178][179][180][181][182][183], as well as determining what signaling pathways may play a role or become dysregulated [184][185][186][187][188][189]. Additionally, other studies have been completed that utilize these cells to examine the role that distinct viral determinants as well as specific host factors have on cellular tropism, cellular differentiation, and cytopathology [190][191][192][193].…”

Section: Hl-60mentioning

confidence: 99%

Myelomonocytic Cell Lines in Modeling HIV-1 Infection of the Bone Marrow

Nonnemacher¹,

Quiterio²,

Allen³

et al. 2017

Biology of Myelomonocytic Cells

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Human immunodeficiency virus type 1 (HIV-1), the etiologic agent of acquired immunodeficiency syndrome (AIDS), primarily infects T cells and cells of the monocyte-macrophage lineage. This is due to the presence of the cell surface receptor CD4 and the coreceptors, CXCR4, and CCR5. While the T-cell has classically been the cell type associated with HIV-1 disease progression, cells of the monocyte-macrophage lineage have also been shown to play a major role in this viral pathologic process. Classically, this has involved monocytic cells in the peripheral blood and tissue macrophages, however, over the course of HIV disease, the promyelomonocytic cells of the bone marrow (BM) have also been shown to play a role in pathogenesis retroviral disease in that they play an integral role in the reseeding of the periphery and end-organ tissues. This has involved an initial infection of the bone marrow hematopoietic progenitor cells. Given this observation, over the years there have been a number of cell lines that have been developed and provided valuable insights into research questions surrounding HIV-1 infection of the monocyte-macrophage cell lineage. In this regard, we will examine the biological and immunological properties of these BM-derived cell lines with respect to their utility in exploring the pathogenesis of HIV-1 in humans.

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Section: Hl-60mentioning

confidence: 99%

Myelomonocytic Cell Lines in Modeling HIV-1 Infection of the Bone Marrow

Nonnemacher¹,

Quiterio²,

Allen³

et al. 2017

Biology of Myelomonocytic Cells

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“…Studies on the stability of protein kinase Cd (25), Hox 2.1 (26), and vascular cell adhesion molecule (27) mRNA have shown a lack of correlation between mRNA half-life and the action of etoposide. Our observation that daunorubicin hydrochloride, etoposide, and vincristine sulfate promoted CYP24 mRNA degradation places these antineoplastic agents in the same category as parathyroid hormone (28) and the anti-HIV protease inhibitor, ritonavir (29), which have been reported to promote CYP24 mRNA instability, thus identifying a novel action of the cytotoxic agents.…”

Section: Effects Of Antineoplastic Agents On the Activity Of The Cyp2mentioning

confidence: 79%

“…Indeed, this concept is supported by a number of observations. Ritonavir, which also inhibits CYP24, increased the intracellular levels of 1,25(OH) 2 D 3 and potentiated the ability of 1,25(OH) 2 D 3 to induce growth arrest and differentiation of HL60 cells (29). Similarly, genistein, ketoconazole, and liarozole, by inhibiting the activity of CYP24 or its expression, can amplify the antiproliferative effects of 1,25(OH) 2 D 3 in DU145 prostate cancer cells (30 -32).…”

Section: Effects Of Antineoplastic Agents On the Activity Of The Cyp2mentioning

confidence: 99%

Antineoplastic agents target the 25-hydroxyvitamin D3 24-hydroxylase messenger RNA for degradation: implications in anticancer activity

Tan

Dwivedi²,

Anderson³

et al. 2007

Molecular Cancer Therapeutics

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Calcitriol or 1,25-dihydroxyvitamin D 3 [1,25(OH) 2 D 3 ] has antitumor activity and hence its levels in patients may play an important role in disease outcome. Here, we report that the antineoplastic agents, daunorubicin hydrochloride, etoposide, and vincristine sulfate inhibited the ability of 1,25(OH) 2 D 3 to cause the accumulation of mRNA for kidney 25-hydroxyvitamin D 3 24-hydroxylase (CYP24), an enzyme which catabolizes this hormone. This was not due to a drug-induced cytotoxic effect, reduction in the expression of the vitamin D receptor or inhibition of the vitamin D receptor -mediated activation of the mitogen-activated protein kinases or CYP24 promoter activity. Interestingly, there was selective degradation of CYP24 mRNA in the presence of the drugs. This was accompanied by an enhancement in the levels of 1,25(OH) 2 D 3 in cells incubated with 25-hydroxy vitamin D 3 . These data identify a novel mechanism of action of some commonly used antineoplastic agents which by decreasing the stability of CYP24 mRNA would prolong the bioavailability of 1,25(OH) 2 D 3 for anticancer actions. [Mol Cancer Ther 2007;6(12):3131 -8]

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“…RNA isolation and cDNA preparation were done as described previously (27). We measured expression of 18S for normalization as previously described (27).…”

Section: Rna Isolation and Real-time Reverse Transcription-polymerasementioning

confidence: 99%

“…We measured expression of 18S for normalization as previously described (27). Realtime reverse transcription-polymerase chain reaction (RT-PCR) was carried out by using Power SyBr Green PCR Master Mix (Applied Biosystems) as described previously (27).…”

Section: Rna Isolation and Real-time Reverse Transcription-polymerasementioning

confidence: 99%

AZ960, a Novel Jak2 Inhibitor, Induces Growth Arrest and Apoptosis in Adult T-Cell Leukemia Cells

Yang

Ikezoe

Nishioka

et al. 2010

Molecular Cancer Therapeutics

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Adult T-cell leukemia/lymphoma (ATL) is a highly aggressive disease in which the Jak2/Stat5 pathway is constitutively activated. This study found that AZ960, a novel inhibitor of Jak2 kinase, effectively induced growth arrest and apoptosis of human T-cell lymphotropic virus type 1, HTLV-1-infected T cells (MT-1 and MT-2) in parallel with downregulation of the phosphorylated forms of Jak2 and Bcl-2 family proteins including Bcl-2 and Mcl-1. Interestingly, AZ960 increased levels of Bcl-xL in MT-1 and MT-2 cells in association with accumulation of cAMP response element-binding protein bound to the Bcl-xL promoter as measured by chromatin immunoprecipitation assay. Importantly, genetic inhibition of Bcl-xL by a small interfering RNA potentiated antiproliferative effects of AZ960 in MT-1 cells. Taken together, Jak2 is an attractive molecular target for treatment of ATL. Concomitant blockade of Jak2 and Bcl-xL may be a promising treatment strategy for this lethal disease. Mol Cancer Ther; 9(12); 3386-95. Ó2010 AACR.

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HIV-1 protease inhibitor ritonavir potentiates the effect of 1,25-dihydroxyvitamin D3 to induce growth arrest and differentiation of human myeloid leukemia cells via down-regulation of CYP24

Cited by 23 publications

References 22 publications

Myelomonocytic Cell Lines in Modeling HIV-1 Infection of the Bone Marrow

Myelomonocytic Cell Lines in Modeling HIV-1 Infection of the Bone Marrow

Antineoplastic agents target the 25-hydroxyvitamin D3 24-hydroxylase messenger RNA for degradation: implications in anticancer activity

AZ960, a Novel Jak2 Inhibitor, Induces Growth Arrest and Apoptosis in Adult T-Cell Leukemia Cells

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