Cross-Resistance to Ionizing Radiation in a Murine Leukemic Cell Line Resistant tocis-Dichlorodiammineplatinum(II): Role of Ku Autoantigen

1999 ◽  
Vol 56 (1) ◽  
pp. 141-146 ◽  
Author(s):  
Philippe Frit ◽  
Yvan Canitrot ◽  
Catherine Muller ◽  
Nicolas Foray ◽  
Patrick Calsou ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Cell Line ◽  
Leukemic Cell ◽  
Cross Resistance ◽  
Leukemic Cell Line ◽  
Ku Autoantigen ◽  
Resistance To Ionizing Radiation

scholarly journals Antisense Long Non-Coding RNA in the LEF1 Locus Regulates Sense LEF1 Expression in Leukemic Cell Line KG1

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 3586-3586
Author(s):  
Ada Congrains ◽  
João Agostinho Machado-Neto ◽  
Flávia Adolfo Corrocher ◽  
Renata Giardini Rosa ◽  
Fernanda Soares Niemann ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cell Differentiation ◽  
Cell Line ◽  
Expression Pattern ◽  
Leukemic Cell ◽  
Leukemic Cell Line ◽  
Over Expression ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Aberrant regulation of the WNT signaling pathway is a signature in numerous human cancers. Lymphoid enhancer-binding factor-1 (LEF1) is an important transcription factor downstream of this pathway. LEF1 over-expression induces AML in mice and plays a critical role in hematopoietic cell differentiation (Petropoulos et al JME 2008). Reduction of LEF1 expression through the progression of myelodysplastic syndrome has been reported and further supports the relevance of this gene in the disease pathogenesis (Pellagatti et al Br J Haematol. 2009). Our previous work using microarray technology revealed a decreased expression of a long non-coding RNA antisense to LEF1 (LEF1-AS) in MDS patients (Baratti et al BMC Medical Genomics 2010). Mounting evidence suggests that long non-coding transcripts play important roles in the epigenetic regulation of coding genes. In this context it is not surprising that long non-coding RNAs are emerging as key players in disease development and progression. Non-coding expression overlapping coding genes is very common and several examples of local regulation have been described in the literature. Here we investigate for the first time the role of LEF1 antisense long non-coding in hematopoiesis and demonstrated its contribution in the regulation of the LEF1 locus in a leukemic cell line. To explore a possible role of LEF1-AS in differentiation, we evaluated the expression pattern of LEF1-AS through erythroid cell differentiation using qRT-PCR. CD34+ HSC cells from 6 healthy donors were induced to differentiate into erythrocytes by addition of erythropoietin during 12 days. We observed that LEF1-AS is modulated during erythroid differentiation. It was significantly down-regulated during the first stages of differentiation from CD34+ HSC to erythroblast (from collection day 6 to day 8 after addition of erythropoietin, 78% mean reduction, P<0.0001) and it was up-regulated at the end-point of collection, day 12 (not significant). Lef1 coding gene displayed a similar expression pattern, consistent with previous reports of Lef1 expression during erythroid maturation (Edmaier et al Leukemia 2014). To explore a possible regulatory role of LEF1-AS, we cloned and over-expressed the transcript in KG1 CD34+ leukemia cell line. Transient over-expression of Lef1-AS led to a significant up-regulation of Lef1 gene (22% increase, P<0.05). We also observed an increase in cell viability (19% increase P<0.05), measured by MTT, which is consistent with the up-regulation of LEF1, a pro-proliferative and anti-apoptotic transcription factor. Our preliminary results from over-expressing LEF1-AS in CD34+ HSCs suggest a similar regulatory effect of LEF1-AS upon its coding counterpart, LEF1. Since aberrant expression of LEF1 is known to disrupt normal differentiation of CD34+ cells, LEF1-AS could potentially affect differentiation through the modulation of LEF1 coding gene. Our results reveal LEF1-AS transcript as a novel player in hematopoiesis and hematologic malignancy. Disclosures No relevant conflicts of interest to declare.

Role of Na+/H+ exchange in the granulocyte-macrophage colony-stimulating factor-dependent growth of a leukemic cell line

1990 ◽  
Vol 143 (1) ◽  
pp. 133-139 ◽  
Author(s):  
Daniele Caracciolo ◽  
Antonella Pannocchia ◽  
Silvia Treves ◽  
Dario Ghigo ◽  
Eugenio Gallo ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemic Cell ◽  
Colony Stimulating Factor ◽  
Leukemic Cell Line ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Dependent Growth ◽  
Stimulating Factor

Characteristics of 25-Hydroxycholesterol-Induced Apoptosis in the Human Leukemic Cell Line CEM

1997 ◽  
Vol 235 (1) ◽  
pp. 35-47 ◽  
Author(s):  
Sylvette Ayala-Torres ◽  
Peter C. Moller ◽  
Betty H. Johnson ◽  
E.Brad Thompson
Keyword(s):  
Cell Line ◽  
Leukemic Cell ◽  
Leukemic Cell Line ◽  
Human Leukemic Cell ◽  
Human Leukemic Cell Line ◽  
Induced Apoptosis

scholarly journals Cis- and trans-repression of class I major histocompatibility gene expression in Abelson virus-transformed murine leukemia

Blood ◽  
1991 ◽  
Vol 78 (2) ◽  
pp. 524-532 ◽  
Author(s):  
RA Zeff ◽  
YF Zhao ◽  
R Tatake ◽  
H Lachman ◽  
F Borriello ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Mhc Class I ◽  
Leukemic Cell ◽  
Class I ◽  
Leukemic Cell Line ◽  
Cis And Trans ◽  
I Gene ◽  
Murine Leukemia ◽  
Mhc Class I Gene

Abstract Numerous tumor cell lines of leukemic origin are known to modulate cell surface expression of major histocompatibility complex (MHC) class I antigens resulting in alterations in their immune detection and tumorigenicity. We have been studying the mechanisms responsible for attenuation of MHC class I gene expression in an H-2 heterozygous (H-2b x H-2d) Abelson-Murine leukemia virus (A-MuLV)-transformed leukemic cell line (designated R8). Here we report that treatment of the R8 cell line with the protein synthesis inhibitor cycloheximide (CHX) increased H-2Kb steady-state messenger RNA (mRNA) levels several fold. The induced H-2Kb mRNA transcripts were functional, as demonstrated by their ability to be translated into immunoprecipitable H-2Kb alloantigen. H-2Kb null variants derived from the R8 cell line were shown to be the product of both cis- and trans-acting mechanisms, insomuch as the treatment of R8-derived H-2Kb non-expressor lines with CHX re-established expression of H-2Kb mRNA to the same extent as transfection of the variant cell line with the wild-type H-2Kb gene. Such findings indicate that downregulation of MHC class I gene expression is constitutive for the R8 leukemic cell line, a phenomenon that may be related to the immature pre-B-cell phenotype of this A-MuLV transformant.

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