Resistance to phorbol 12-myristate 13-acetate-induced cell growth arrest in an HL60 cell line chronically exposed to a glutathione S-transferase π inhibitor

Gaté, Laurent; Lunk, Alexandra; Tew, Kenneth D.

doi:10.1016/s0006-2952(03)00152-7

Cited by 12 publications

(4 citation statements)

References 16 publications

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“…In malignant cells, including breast cancer cells [48], HeLa cells [49] and human colon cancer cells [50], drug treatment was reported to cause 14-3-3 up-regulation. GSTP1 is a regulator of mitogen-activated protein kinases (MAPK), and is correlated with cell cycle G1 phase arrest in drug treated cancer cells [51]. Galectin-1 has been shown to suppress tumor cell growth by activating the cyclin-dependent kinase inhibitors (CKI) p21 and p27 [52].…”

Section: Discussionmentioning

confidence: 99%

Endogenous HIV-1 Vpr-mediated apoptosis and proteome alteration of human T-cell leukemia virus-1 transformed C8166 cells

Zeng

et al. 2009

Apoptosis

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HIV-1 viral protein R (Vpr) can induce cell cycle arrest and cell death, and may be beneficial in cancer therapy to suppress malignantly proliferative cell types, such as adult T-cell leukemia (ATL) cells. In this study we examined the feasibility of employing the HIV-vpr gene, via targeted gene transfer, as a potential new therapy to kill ATL cells. We infected C8166 cells with a recombinant adenovirus carrying both vpr and GFP genes (rAd-vpr), as well as the vector control virus (rAd-vector). G2/M phase cell cycle arrest was observed in the rAd-vpr infected cells. Typical characteristics of apoptosis were detected in rAd-vpr infected cells, including sub-diploid peak exhibition in DNA content assay, the Hoechst 33342 accumulation, apoptotic body formation, mitochondrial membrane potential and plasma membrane integrity loss. The proteomic assay revealed apoptosis related protein changes, exhibiting the regulation of caspase-3 activity indicator proteins (vimentin and Rho GDP-dissociation inhibitor 2), mitochondrial protein (prohibitin) and other regulatory proteins. In addition, the up-regulation of anti-inflammatory redox protein, thioredoxin, was identified in the rAd-vpr infected group. Further supporting these findings, the increase of caspase 3&7 activity in the rAd-vpr infected group was observed. In conclusion, endogenous Vpr is able to kill HTLV-1 transformed C8166 cells, and may avoid the risks of inducing severe inflammatory responses through apoptosis-inducing and anti-inflammatory activities.

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Section: Discussionmentioning

confidence: 99%

Endogenous HIV-1 Vpr-mediated apoptosis and proteome alteration of human T-cell leukemia virus-1 transformed C8166 cells

Zeng

et al. 2009

Apoptosis

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“…Further differentiation of these lines can be induced by various agents, for example, all-trans retinoic acid (ATRA) and phorbol 12-myristate 13-acetate (PMA) [1][2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Effect of differentiating agents (all-trans retinoic acid and phorbol 12-myristate 13-acetate) on drug sensitivity of HL60 and NB4 cells in vitro.

Jasek

Mirecka²,

Litwin³

2008

Folia Histochem Cytobiol.

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Abstract:In vitro studies have shown that human myeloid leukemia cell lines: HL60 and NB4 can be stimulated to differentiation by various agents, for example, all-trans retinoic acid (ATRA) and phorbol 12-myristate 13-acetate (PMA). The purpose of this study was to investigate whether differentiation of HL60 and NB4 leukemia cell lines induced by ATRA and PMA alters their drug sensitivity. The differentiation along the neutrophil lineage (upon stimulation with ATRA) and along the monocyte/macrophage lineage (upon stimulation with PMA) was proved by decreased proliferative potential of cells, changes in their morphology, increased ability for NBT reduction and increased expression of CD11b and CD14 cell surface markers. The effect of drugs: cytosine arabinoside, daunorubicin, mitoxantrone and etoposide was examined by Alamar Blue test (proliferation and survival rates), as well as by evaluation of cell smears stained with Hoechst 33342 (apoptotic index). Differentiation resulted in the change of drug sensitivity in both cell lines: the differentiation along the neutrophil pathway (after stimulation with ATRA) increased sensitivity to cytosine arabinoside and mitoxantrone but decreased sensitivity to etoposide; the differentiation along the monocyte/macrophage pathway (induced by PMA) resulted in the decreased sensitivity of both cell lines to all drugs tested. In conclusion, we have shown that ATRA-and PMA-mediated differentiation of HL60 and NB4 cell lines results in the changes of their drug sensitivity. Our data may provide a contribution to a strategy aimed at a rational combination of differentiating agents and conventional anticancer drugs.

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“…Especially, the absence of CD14 which is normally found on tissue macrophages is attributed to inefficiency of TPA induction and it is accepted that phorbol esters not to significantly induce CD14 on HL60 cells [2][3][4]. However, Gaté et al [13] reported that in response to PMA, *40% of plastic-adherent HL60 cells express CD14. In association with TLR4 and TLR2, membrane-bound CD14 functions as a receptor for lipopolysaccharide (LPS) [11].…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, like undifferentiated HL60, macrophage-like cells generated with phorbol esters are not able to efficiently reduce NBT, while monocytic or granulocytic differentiation results in ROS production [13,18]. Following the treatment with PMA, phagocytic activity and ROS production was prominently enhanced in fibronectinadherent HL60 cells.…”

Section: Discussionmentioning

confidence: 99%

Fibronectin promotes the phorbol 12-myristate 13-acetate-induced macrophage differentiation in myeloid leukemia cells

et al. 2009

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The extracellular matrix plays a critical role in macrophage maturation. In this study, the HL60 cell line was used as a model of leukemic myeloid cell differentiation. We assessed the ability of HL60 cells cultured on fibronectin substratum prior to phorbol 12-myristate 13-acetate (PMA) induction to differentiate into terminally differentiated macrophages. Beside their distinctive macrophage morphology, they expressed antigen receptors CD14, TLR2, TLR4 and CD68, and displayed enhanced phagocytic activity and production of reactive oxygen species. Expression of CD13, CD33, CD15 and alpha-naphthyl-acetate esterase was also maintained, however, differentiated HL60 cells were HLA-DR and CD1a negative. Here, we describe the enhanced capacity of fibronectin-adherent HL60 cells to differentiate into macrophages in response to PMA.

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Resistance to phorbol 12-myristate 13-acetate-induced cell growth arrest in an HL60 cell line chronically exposed to a glutathione S-transferase π inhibitor

Cited by 12 publications

References 16 publications

Endogenous HIV-1 Vpr-mediated apoptosis and proteome alteration of human T-cell leukemia virus-1 transformed C8166 cells

Endogenous HIV-1 Vpr-mediated apoptosis and proteome alteration of human T-cell leukemia virus-1 transformed C8166 cells

Effect of differentiating agents (all-trans retinoic acid and phorbol 12-myristate 13-acetate) on drug sensitivity of HL60 and NB4 cells in vitro.

Fibronectin promotes the phorbol 12-myristate 13-acetate-induced macrophage differentiation in myeloid leukemia cells

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