scholarly journals Comparison of Effects of the Ethanolic Extracts of Brazilian Propolis on Human Leukemic Cells As Assessed with the MTT Assay

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Gilberto C. Franchi ◽  
Cleber S. Moraes ◽  
Viviane C. Toreti ◽  
Andreas Daugsch ◽  
Alexandre E. Nowill ◽  
...  
Keyword(s):  
K562 Cells ◽  
Leukemic Cells ◽  
Cytotoxic Activities ◽  
Human Leukemia ◽  
Cancer Cell Growth ◽  
Brazilian Propolis ◽  
Human Leukemic Cells ◽  
Dioxin Toxicity ◽  
Resinous Product

Propolis is a resinous product collected by honey bees. It was also reported that propolis has a wide variety of biological actions, including antimicrobial activity and antioxidant, anti-inflammatory, and suppressive effects of dioxin toxicity activities. The aim of this study was to compare the in vitro cytotoxic activities of green propolis (G12) and red propolis (G13) in human leukemia cells. These cells were incubated with different concentrations of propolis and 48 hours after the IC50was calculated for each cell. The results showed that the red propolis has cytotoxic effect in vitro higher than green propolis. Red propolis was showed to be cytostatic in K562 cells and caused the same amount of apoptosis as its control Gleevec. In conclusion, these results showed that red propolis is more cytotoxic than the green propolis in a variety of human cell lines of leukemia. Red propolis may contain drugs capable of inhibiting cancer cell growth. Therefore, further isolation of respective chemical ingredients from the red propolis (G13) for identification of the activities is necessary.

scholarly journals The in vitro synthesis of polypeptides for the platelet membrane glycoproteins IIb and IIIa

Blood ◽  
1987 ◽  
Vol 69 (4) ◽  
pp. 1031-1037 ◽  
Author(s):  
SM Silver ◽  
MM McDonough ◽  
G Vilaire ◽  
JS Bennett
Keyword(s):  
Leukemia Cell ◽  
K562 Cells ◽  
Platelet Membrane ◽  
Human Leukemia ◽  
Membrane Glycoproteins ◽  
In Vitro Synthesis ◽  
Calcium Dependent ◽  
Hel Cells ◽  
Von Willebrand

Abstract The platelet membrane glycoproteins IIb (GpIIb) and GpIIIa form calcium- dependent heterodimers containing binding sites for fibrinogen, von Willebrand factor, and fibronectin. Although GpIIb and GpIIIa are distinct proteins, both GpIIb and GpIIIa are deficient in platelets from individuals with the recessive disorder Glanzmann's thrombasthenia. To gain a better understanding of the genetic basis for GpIIb and GpIIIa synthesis, we studied their synthesis by two human leukemia cell lines, HEL and K562. HEL cells contained complexes of GpIIb and GpIIIa, and K562 cells expressed GpIIIa, but not GpIIb, when stimulated with phorbol-12-myristate-13-acetate (PMA). RNA from HEL cells directed the in vitro synthesis of a 110,000-Mr precursor for GpIIb and a 92,000-Mr precursor for GpIIIa, which indicates that the synthesis of GpIIb and GpIIIa by HEL cells is directed by separate mRNAs. In contrast, RNA from PMA-stimulated K562 cells only directed the synthesis of a 92,000-Mr precursor for GpIIIa. The dissociation of GpIIb and GpIIIa synthesis in K562 cells suggests that GpIIb and GpIIIa may be the products of separate genes.

CFTR in K562 human leukemic cells

2003 ◽  
Vol 285 (2) ◽  
pp. C480-C488 ◽  
Author(s):  
Yanina A. Assef ◽  
Alicia E. Damiano ◽  
Elsa Zotta ◽  
Cristina Ibarra ◽  
Basilio A. Kotsias
Keyword(s):  
Single Channel ◽  
Functional Characterization ◽  
Leukemic Cells ◽  
Cftr Gene ◽  
Human Leukemia ◽  
Selectivity Ratio ◽  
Open Probability ◽  
Selective Channel ◽  
Human Leukemic Cells

In this study, the expression and functional characterization of CFTR (cystic fibrosis transmembrane regulator) was determined in K562 chronic human leukemia cells. Expression of the CFTR gene product was determined by RT-PCR and confirmed by immunohistochemistry and Western blot analysis. Functional characterization of CFTR Cl- channel activity was conducted with patch-clamp techniques. Forskolin, an adenylyl cyclase activator, induced an anion-selective channel with a linear current-voltage relationship and a single-channel conductance of 11 pS. This cAMP-activated channel had a Pgluconate/PCl or PF/PCl perm-selectivity ratio of 0.35 and 0.30, respectively, and was inhibited by the CFTR blocker glibenclamide and the anti-CFTR antibody MAb 13-1, when added to the cytoplasmatic side of the patch. Glibenclamide decreased the open probability increasing the frequency of open-to-closed transitions. Addition of 200 μM DIDS caused an irreversible block of the channels when added to the cytosolic side of inside-out patches. These and other observations indicate a widespread distribution of CFTR gene expression and suggest that this channel protein may function in most human cells to help maintain cellular homeostasis.

Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification

Blood ◽  
2000 ◽  
Vol 95 (5) ◽  
pp. 1758-1766 ◽  
Author(s):  
Philipp le Coutre ◽  
Elena Tassi ◽  
Marileila Varella-Garcia ◽  
Rossella Barni ◽  
Luca Mologni ◽  
...  
Keyword(s):  
Cell Line ◽  
Gene Amplification ◽  
Marker Chromosome ◽  
Kinase Domain ◽  
Leukemic Cells ◽  
Tyrosine Kinase Domain ◽  
Fish Analysis ◽  
Human Leukemic Cells

The 2-phenylaminopyrimidine derivative STI571 has been shown to selectively inhibit the tyrosine kinase domain of the oncogenicbcr/abl fusion protein. The activity of this inhibitor has been demonstrated so far both in vitro with bcr/abl expressing cells derived from leukemic patients, and in vivo on nude mice inoculated with bcr/abl positive cells. Yet, no information is available on whether leukemic cells can develop resistance to bcr/ablinhibition. The human bcr/abl expressing cell line LAMA84 was cultured with increasing concentrations of STI571. After approximately 6 months of culture, a new cell line was obtained and named LAMA84R. This newly selected cell line showed an IC50 for the STI571 (1.0 μM) 10-fold higher than the IC50 (0.1 μM) of the parental sensitive cell line. Treatment with STI571 was shown to increase both the early and late apoptotic fraction in LAMA84 but not in LAMA84R. The induction of apoptosis in LAMA84 was associated with the activation of caspase 3–like activity, which did not develop in the resistant LAMA84R cell line. LAMA84R cells showed increased levels of bcr/abl protein and mRNA when compared to LAMA84 cells. FISH analysis with BCR- and ABL-specific probes in LAMA84R cells revealed the presence of a marker chromosome containing approximately 13 to 14 copies of the BCR/ABL gene. Thus, overexpression of the Bcr/Abl protein mediated through gene amplification is associated with and probably determines resistance of human leukemic cells to STI571 in vitro.

scholarly journals cis-Retinoic acid stimulates the clonal growth of some myeloid leukemia cells in vitro

Blood ◽  
1987 ◽  
Vol 69 (1) ◽  
pp. 302-307 ◽  
Author(s):  
HJ Lawrence ◽  
K Conner ◽  
MA Kelly ◽  
MR Haussler ◽  
P Wallace ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
T Lymphocytes ◽  
Clonal Growth ◽  
Colony Growth ◽  
Leukemic Cells ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Growth Responses ◽  
Drug Concentrations

Abstract We studied the effects of cis-retinoic acid (cisRA) on the clonogenic growth of samples of leukemic cells from 35 patients with acute nonlymphocytic leukemia (ANLL). We observed significant inhibition of leukemic colony growth in 17 samples by 10(-7) to 10(-6)M cisRA. However, we found that retinoid exposure resulted in striking stimulation of clonal growth in ten samples at the same drug concentrations. With the exception of cases with promyelocytic features, there was no morphologic or functional evidence that cisRA induced the leukemic blasts to differentiate. Both inhibition and stimulation were dose-dependent and observable at pharmacologically achievable levels of cisRA. Leukemic cells with monocytic features more frequently demonstrated a stimulatory response than did those without monocytic features. Depletion of T lymphocytes and monocytes did not alter the type of growth response. Assays for cellular retinoic acid- binding protein (CRABP) were performed on five samples (two with inhibitory growth responses, two with stimulatory responses, and one with no growth) and failed to reveal detectable levels of CRABP in any case. The addition of cisRA to liquid suspensions of leukemic cells produced no significant change in the number of viable cells. We conclude that the effects of cisRA on leukemic colony growth are not cytotoxic and not mediated by T lymphocytes, monocytes, or CRABP. More importantly, cisRA appears to enhance the growth of certain human leukemia cells in vitro. Taking into account the increasing use of retinoids in clinical trials for patients with leukemia, the latter findings may represent a significant cautionary note.

scholarly journals Curcumin and Its Analogue Induce Apoptosis in Leukemia Cells and Have Additive Effects with Bortezomib in Cellular and Xenograft Models

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
L. I. Nagy ◽  
L. Z. Fehér ◽  
G. J. Szebeni ◽  
M. Gyuris ◽  
P. Sipos ◽  
...  
Keyword(s):  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Leukemia Cells ◽  
Great Promise ◽  
Human Leukemia ◽  
Human Leukemia Cell Line ◽  
Apoptotic Effects

Combination therapy of bortezomib with other chemotherapeutics is an emerging treatment strategy. Since both curcumin and bortezomib inhibit NF-κB, we tested the effects of their combination on leukemia cells. To improve potency, a novel Mannich-type curcumin derivative, C-150, was synthesized. Curcumin and its analogue showed potent antiproliferative and apoptotic effects on the human leukemia cell line, HL60, with different potency but similar additive properties with bortezomib. Additive antiproliferative effects were correlated well with LPS-induced NF-κB inhibition results. Gene expression data on cell cycle and apoptosis related genes, obtained by high-throughput QPCR, showed that curcumin and its analogue act through similar signaling pathways. In correlation with in vitro results similar additive effect could be obsereved in SCID mice inoculated systemically with HL60 cells. C-150 in a liposomal formulation given intravenously in combination with bortezomib was more efficient than either of the drugs alone. As our novel curcumin analogue exerted anticancer effects in leukemic cells at submicromolar concentration in vitro and at 3 mg/kg dose in vivo, which was potentiated by bortezomib, it holds a great promise as a future therapeutic agent in the treatment of leukemia alone or in combination.

Impaired Expression of the DNA Repair Factor DDB2 in Human Myeloid Leukemias.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 2046-2046
Author(s):  
Rishu Takimoto ◽  
Junji Kato ◽  
Koichi Takada ◽  
Takuya Matsunaga ◽  
Yoshiro Niitsu
Keyword(s):  
Dna Repair ◽  
Excision Repair ◽  
Leukemia Cell ◽  
K562 Cells ◽  
Leukemic Cells ◽  
Repair System ◽  
Myeloid Leukemias ◽  
Repair Factor ◽  
Human Leukemic Cells ◽  
Damaged Dna

Abstract Recent studies have suggested that chromosomal deletions might represent a mechanism of inactivation of DNA repair system in various hematological malignancies, including myeloid leukemias. However, the precise mechanisms remain unclear. Damaged DNA binding protein-2 (DDB2), a DNA repair factor induced by tumor suppressor p53, plays an important role in the nucleotide excision repair of UV-damaged DNA. Despite frequent mutations of p53 in human leukemic cells, the role of DDB2 on the leukemogenesis is unkown. In this study, we examined expression of DDB2 mRNA in four human myeloid leukemia cell lines (K562, KG1, HL60, and MEG01) and in fresh leukemic cells obtained from 4 patients with myeloid leukemias. In all leukemia cells, expression of DDB2 mRNA was remarkably decreased as compared to that of CD34 cells We then assayed DDB2-dependent DNA repairing activity in the leukemic cells using specific antibodies against photoproducts, and found that DNA repairing activity was reduced. When a plasmid encoding DDB2 gene (pCV-DDB2) was transduced into K562 cells, the DNA repairing activity was significantly restored. Finally we tested the expression of DDB2 mRNA in five myeloid leukemias obtained from patients, and found loss of DDB2 expression in four patients. These results suggested that in human myeloid leukemias, suppression of DDB2 expression may contribute to accumulation of gene mutation through the dysfunction of DNA repair.

scholarly journals Vitamin E in Chronic Myeloid Leukemia (CML) Prevention

2021 ◽  
Author(s):  
Lyudmyla Shvachko ◽  
Michael Zavelevich ◽  
Daniil Gluzman ◽  
Gennadii Telegeev
Keyword(s):  
Alkaline Phosphatase ◽  
Vitamin E ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Blast Crisis ◽  
K562 Cells ◽  
Leukemic Cells ◽  
Blast Cells ◽  
Differentiation Block

The resistance to inhibitors of tyrosine kinase necessitates novel approaches to the therapy of chronic myeloid leukemia (CML). The progression of CML to blast crisis is associated with down-regulation of C/EBP-alpha being involved in the differentiation block in leukemic blast cells. Moreover, lowered C/EBP-alpha expression correlates with resistance to imatinib in CML. We have demonstrated that vitamin E up-regulates expression of C/EBP-alpha and down-regulates expression of Snail transcription factor in K562 cells in vitro contributing to the putative recovery of myeloid differentiation potential. In parallel with increased CEBP alpha expression, Vitamin E treatment results in the decreasing expression of placental-like alkaline phosphatase and increasing expression of tissue non-specific alkaline phosphatase. We suggest that vitamin E could be used as the plausible biological modulator to prevent the progression to blast crisis and to overcome drug resistance of leukemic cells in CML.

scholarly journals Proliferation and differentiation of human myeloid leukemic cells in immunodeficient mice: electron microscopy and cytochemistry

Blood ◽  
1984 ◽  
Vol 63 (5) ◽  
pp. 1015-1022 ◽  
Author(s):  
EA Machado ◽  
DA Gerard ◽  
CB Lozzio ◽  
BB Lozzio ◽  
JR Mitchell ◽  
...  
Keyword(s):  
Nude Mice ◽  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Immunodeficient Mice ◽  
Human Leukemia Cells

Abstract To study the influence of a biologic environment on cultured human leukemia cells, KG-1, KG-1a, and HL-60 cells were inoculated subcutaneously into newborn nude mice. The cells developed myelosarcomas at the site of inoculation and in lungs and kidneys. KG-1 and HL-60 myelosarcomas were successfully passaged through adult nude mice, whereas KG-1a tumors proliferated only after transplantation into newborn hosts. The human nature of the cells forming myelosarcomas in mice was assessed by chromosomal analyses and detection of cross- reactivity with an antibody to the human leukemia cell line K562. We undertook electron microscopic and cytochemical examinations of the cells proliferating in vitro and in the mice. The granules of KG-1 cells in vivo did not react for acid phosphatase, as observed in vitro, and the HL-60 cells proliferating in mice lost the perinuclear myeloperoxidase (MPO) demonstrated in cultured cells. Although the influence of an in vivo selection of cell subpopulations cannot be ruled out, the enzymatic changes are compatible with induced cell differentiation. Conclusive evidence of differentiation in vivo was observed in the KG-1a cell subline. The undifferentiated KG-1a blasts developed cytoplasmic granules and synthesized MPO during proliferation in vivo. These observations indicate that human leukemia cells from established cell lines proliferate in nude mice and may acquire new differentiated properties in response to the in vivo environment.

scholarly journals 5-Aza-2'-deoxycytidine induces terminal differentiation of leukemic blasts from patients with acute myeloid leukemias

Blood ◽  
1984 ◽  
Vol 64 (4) ◽  
pp. 922-929 ◽  
Author(s):  
A Pinto ◽  
V Attadia ◽  
A Fusco ◽  
F Ferrara ◽  
OA Spada ◽  
...  
Keyword(s):  
Suspension Culture ◽  
Terminal Differentiation ◽  
Functional Differentiation ◽  
Leukemic Cells ◽  
In Vitro Differentiation ◽  
Myeloid Leukemias ◽  
Human Leukemic Cells ◽  
First Time ◽  
Acute Myeloid

Abstract In this study, the effects of 5-aza-2′-deoxycytidine on differentiation of human leukemic cells in primary suspension culture are reported for the first time. Morphological and functional differentiation was induced in cells from two acute monoblastic leukemias and two of three acute myeloid leukemias following repeated exposures to 1 mumol/L 5-aza- 2′-deoxycytidine. The observation that nontoxic concentrations of the drug are able to induce the in vitro differentiation of both monoblastic and myeloblastic leukemic cells into mature elements may encourage the exploitation of the differentiating properties of 5-aza- 2′-deoxycytidine in chemotherapy protocols for acute non-lymphoblastic leukemias.

Sign in / Sign up

Export Citation Format

Share Document