In vitro culture with prednisolone increases BCL-2 protein expression in adult acute lymphoblastic leukemia cells

Tosi, Patrizia; Visani, Giuseppe; Ottaviani, Emanuela; Manfroi, Silvia; Tura, S

doi:10.1002/(sici)1096-8652(199604)51:4<261::aid-ajh2>3.0.co;2-u

Cited by 6 publications

(3 citation statements)

References 15 publications

(14 reference statements)

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“…This finding was unexpected since we had speculated that exposure of myeloma cells to anti-cancer agents might induce expression of Bcl-2. Indeed, expression of Bcl-2 was reported to be induced by exposure of leukemia cells to steroids, 13 and in vitro experiments showed that a high level of expression of Bcl-2 is known to mediate drug resistance. 2 Although analysis of more cases and further in vitro studies are necessary to clarify the phenomenon, the initial levels of expression of Bcl-2 and Bcl-X L may be more important than the induction of these proteins by chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Expression of Bcl-2 family of proteins in fresh myeloma cells

et al. 1998

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Section: Discussionmentioning

confidence: 99%

Expression of Bcl-2 family of proteins in fresh myeloma cells

et al. 1998

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“…Also analysing Bcl-2 protein expression, Klampfer et al [36], demonstrated that treatment with sodium salicylate after 5 and 18 h did not alter the expression of the Bcl-2 proteins in the TF-1 acute myeloid leukaemia cell line. However, several authors reported that Bcl-2 protein expression in some tumoral cells is enhanced by chemotherapeutic drugs [41]. In relation to the biological model used in the present work, Zhang et al [34] observed that indomethacin (NSAID) down-regulates bcl-2 gene expression in K562 cells.…”

Section: Discussionmentioning

confidence: 66%

Anti-MDR and antitumoral action of acetylsalicylic acid on leukaemic cells

et al. 2011

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ASA (acetylsalicylic acid) is an NSAID (non-steroidal anti-inflammatory drug). ASA has gained attention as a potential chemopreventive and chemotherapeutic agent for several neoplasms. The aim of this study was to analyse the possible antitumoural effects of ASA in two erythroleukaemic cell lines, with or without the MDR (multidrug resistance) phenotype. The mechanism of action of different concentrations of ASA were compared in K562 (non-MDR) and Lucena (MDR) cells by analysing cell viability, apoptosis and necrosis, intracellular ROS (reactive oxygen species) formation and bcl-2, p53 and cox-2 gene expression. ASA inhibited the cellular proliferation or induced toxicity in K562 and Lucena cell lines, irrespective of the MDR phenotype. The ASA treatment provoked death by apoptosis and necrosis in K562 cells and only by necrosis in Lucena cells. ASA also showed antioxidant activity in both cell lines. The bcl-2, p53 and cox-2 genes in both cell lines treated with ASA seem to exhibit different patterns of expression. However, normal lymphocytes treated with the same ASA concentrations were more resistant than tumoral cells. The results of this work show that both cell lines responded to treatment with ASA, demonstrating a possible antitumoral and anti-MDR role for this drug.

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“…Bcl-2 up-regulation has not yet been reported to occur after in vivo administration of chemotherapeutic agents (Walton et al, 1993). Tosi et al (1996) have recently observed increased bcl-2 expression after prednisolone in vitro. In these studies, we show that high-dose HN2 up-regulates bcl-2 protein levels both in HT-29, a cell line that normally has low bcl-2 levels, and in MCF-7, a cell line normally expressing high levels of bcl-2.…”

Section: Discussionmentioning

confidence: 96%

Nitrogen mustard up-regulates Bcl-2 and GSH and increases NTP and PCr in HT-29 colon cancer cells

Boddie

Constantinou²,

Williams³

et al. 1998

Br J Cancer

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Summary We hypothesized that unexplained increases in nucleoside triphosphates (NTP) observed by 31 magnetic resonance spectroscopy (MRS) after treatment of tumours by DNA-damaging agents were related to chemotherapy-induced up-regulation of the bcl-2 gene and DNA damage prevention and repair processes. To test this hypothesis, we treated HT-29 cells with 10-4 M nitrogen mustard (HN2) and performed sequential perchloric acid extractions in replicate over 0-18 h. By reference to an intemal standard (methylene diphosphonic acid), absolute changes in 31P-detectable high-energy phosphates in these extracts were determined and correlated with changes in bcl-2 protein levels, cell viability, cell cycle, apoptosis and total cellular glutathione (GSH) (an important defence against DNA damage from alkylating agents). After HN2 administration, bcl-2 protein levels in the HT-29 cell line rose at 2 h. Cell viability declined to 25% within 18 h, but apoptosis measured using fluorescence techniques remained in the 1-4% range. Increased cell division was noted at 4 h. Two high-energy interconvertible phosphates, NTP (P < 0.006) and phosphocreatine (PCr) (P < 0.0002), increased at 2 h concurrently with increased levels of bcl-2 protein and glutathione. This study demonstrates that bcl-2 and glutathione are up-regulated by HN2 and links this to a previously unexplained 31p MRS phenomenon: increased NTP after chemotherapy.

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In vitro culture with prednisolone increases BCL-2 protein expression in adult acute lymphoblastic leukemia cells

Cited by 6 publications

References 15 publications

Expression of Bcl-2 family of proteins in fresh myeloma cells

Expression of Bcl-2 family of proteins in fresh myeloma cells

Anti-MDR and antitumoral action of acetylsalicylic acid on leukaemic cells

Nitrogen mustard up-regulates Bcl-2 and GSH and increases NTP and PCr in HT-29 colon cancer cells

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