scholarly journals The Levels of Leukemia Inhibitory Factor mRNA in a Schwann Cell Line Are Regulated by Multiple Second Messenger Pathways

2008 ◽  
Vol 72 (5) ◽  
pp. 1871-1881 ◽  
Author(s):  
Kumi Nagamoto-Combs ◽  
Stacey A. Vaccariello ◽  
Richard E. Zigmond
Keyword(s):  
Schwann Cell ◽  
Cell Line ◽  
Leukemia Inhibitory Factor ◽  
Second Messenger ◽  
Inhibitory Factor ◽  
Second Messenger Pathways

An In Vitro and In Vivo Evidence That Downregulation of Leukemia Inhibitory Factor (LIF) Receptor (LIF-R) Decreases the Metastatic Potential of Human Rhabdomyosarcoma (RMS) Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2561-2561
Author(s):  
Marcin Wysoczynski ◽  
Katarzyna Miekus ◽  
Anna Marcinkowska ◽  
Anna Janowska-Wieczorek ◽  
Mariusz Z. Ratajczak
Keyword(s):  
Skeletal Muscle ◽  
Bone Marrow ◽  
Cell Line ◽  
Cell Lines ◽  
Leukemia Inhibitory Factor ◽  
Biological Significance ◽  
Human Cells ◽  
Inhibitory Factor

Abstract Rhabdomyosarcoma (RMS) and skeletal muscle-derived tumors frequently infiltrate bone marrow (BM). We have demonstrated that the stromal-derived factor (SDF)-1-CXCR4 receptor (Blood2002;100:2597) and hepatocyte growth factor (HGF)-c-Met receptor (Cancer Res. 2003;63:7926) play an important role in RMS metastasis to BM. Leukemia inhibitory factor (LIF) is a well known factor that plays an important role in skeletal muscle development/regeneration and similarly as SDF-1 and HGF is secreted by BM stroma. This prompted us to examine whether the LIF-LIF receptor (LIF-R) axis affects the biology/metastasis of RMS cells. We employed in our studies, human established RMS cell lines, as well as RMS samples isolated from patients and noticed that LIF-R was expressed not only on established human RMS cell lines (7/7) but more importantly, it was also detectable in patient samples (23/23). We also found that in RMS cells LIF stimulatesphosphorylation of MAPKp42/44, AKT and STAT3,chemotaxis and adhesion andincreases resistance to cytostatics (e.g., etoposide). These LIF-mediated effects were inhibited after downregulating the LIF-R by siRNA. To learn more on the biological significance of the LIF-LIF-R axis in vivo we employed two models. First, human RMS cells (RH-30) were exposed or not exposed to LIF-R siRNA and subsequently injected into SCID™-Beige immunodeficient mice. To estimate the number of RMS cells that seed to BM and liver in these animals, we isolated DNA and using real- time RT-PCR, amplified human a-satellite sequences and murine b-actin. The number of human cells present in murine organs was subsequently calculated from a standard curve derived from mixing varying numbers of human cells with a constant number of murine cells. We noticed that downregulation of LIF-R by siRNA significantly decreased the number of human RMS cells in murine BM and liver (x4 and x2 respectively). In a second model, the RH30 cell line was selected by repetitive chemotaxis for cells that are highly responsive to LIF (RH-30 L) and subsequently the cells from parental RH-30 cell line and RH-30 L cells were injected intramuscularly. Six weeks after tumour inoculation, we detected more metastasis in bone marrow and lungs in mice injected with RH-30L cells as compared to parental RH-30 clone (x6 and x3 respectively). In conclusion, we present evidence for the first time that the inhibition of LIF-LIF-R axis may decrease the invasive potential of human RMS both in vitro and in vivo. Hence, molecular targeting of LIF-LIF-R axis could possibly become a more effective new strategy to control the progression and metastasis of RMS.

Leukemia inhibitory factor mRNA is expressed in cortical astrocyte cultures but not in an immortalized microglial cell line

1995 ◽  
Vol 184 (1) ◽  
pp. 48-51 ◽  
Author(s):  
Greer M Murphy ◽  
Yaoli Song ◽  
Elisa Ong ◽  
Yuen Ling Lee ◽  
Karen G Schraidt ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemia Inhibitory Factor ◽  
Microglial Cell ◽  
Inhibitory Factor ◽  
Cortical Astrocyte ◽  
Microglial Cell Line

scholarly journals The Effects of the Trifolium Pratense L. Extract on the Leukemia Inhibitory Factor and its Receptor in The Endometrial Epithelial Cell Line

2021 ◽  
Vol 16 (10) ◽  
pp. 1934578X2110454
Author(s):  
Sibel Kokturk ◽  
Fatma Kaya Dagistanli ◽  
Sibel Dogan ◽  
Emel Usta ◽  
Hatice Colgecen ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemia Inhibitory Factor ◽  
Trifolium Pratense ◽  
Endometrial Adenocarcinoma ◽  
Staining Intensity ◽  
Inhibitory Factor ◽  
Epithelial Cell Line ◽  
Endometrial Epithelial Cell ◽  
Ishikawa Cells ◽  
Trifolium Pratense L

Isoflavones have attracted much notice due to their health advantages; however, a comprehensive understanding of the effects of isoflavones on endometrium biology remains undiscovered. The expression and deficiency of leukemia inhibitory factor (LIF) and LIF receptor (LIFR) has been shown to be involved in multiple implantations failures in female infertility. Mechanisms implicated in the failure of implantations require further researches, thus our aim is to investigate the effect of the Trifolium pratense L. isoflavone extract with abundant formononetin content on implantation through assessing LIF and LIFR expressions. The Ishikawa cells were cultured with 20, 30, and 40 µg/mL concentrations of Trifolium pratense L. isoflavone extracts for 24 h and detected staining intensity of LIF and LIFR by immunocytochemistry and immunofluorescence staining using image analysis software. As compared with the control and 20 µg/mL Trifolium pratense L. groups, the staining intensity of LIF and LIFR in 30 and 40 µg/mL Trifolium pratense L. groups were significantly increased ( P < .0001). Our findings suggest that Trifolium pratense L. isoflavone extract may alter the endometrium expression of LIF and LIFR in the human endometrial adenocarcinoma cell line.

Buffalo Leukemia Inhibitory Factor Induces Differentiation and Dome-Like Secondary Structures in COS-1 Cells

2017 ◽  
Vol 151 (3) ◽  
pp. 119-130 ◽  
Author(s):  
Gurjeet Kaur ◽  
Syed Azmal Ali ◽  
Shikha Pachauri ◽  
Dhruba Malakar ◽  
Jai K. Kaushik ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemia Inhibitory Factor ◽  
Functional Characterization ◽  
Cumulus Cells ◽  
Secondary Structures ◽  
Inhibitory Factor ◽  
Molecular Characteristics ◽  
Multiple Sequence ◽  
Reading Frame ◽  
Qrt Pcr

This study aimed to understand the molecular characteristics of buffalo leukemia inhibitory factor (BuLIF) and the generation of a stably transfected COS-1_BuLIF cell line for its functional characterization. Cumulus cells, isolated from oocytes, were separated, and total cDNA was prepared. The BuLIF gene was ligated into the cloning vector pJET1.2/blunt and expression vector pAcGFP-N1 which was transfected into COS-1 cells and confirmed by qRT-PCR and Western blot. BuLIF was immunoprecipitated and evaluated through a MTT assay. qRT-PCR of STAT3 was performed. The multiple sequence alignment of BuLIF showed high similarity with sheep (98.77%) and cattle (96.62%) compared with other species. The BuLIF gene has an open reading frame of 609 nucleotides coding for 202 amino acids. BuLIF was integrated into the genome of COS-1 cells and resulted in the formation of dome-like secondary structures which are indicative of its functional role mediated through STAT3 proteins. In conclusion, this cell line is suitable for understanding LIF-mediated biological functions.

scholarly journals Reversal of Glucocorticoids-Dependent Proopiomelanocortin Gene Inhibition by Leukemia Inhibitory Factor

Endocrinology ◽  
2007 ◽  
Vol 148 (1) ◽  
pp. 422-432 ◽  
Author(s):  
Olivier Latchoumanin ◽  
Vanessa Mynard ◽  
Jocelyne Devin-Leclerc ◽  
Marie-Annick Dugué ◽  
Xavier Bertagna ◽  
...  
Keyword(s):  
Cell Line ◽  
Leukemia Inhibitory Factor ◽  
Molecular Mechanisms ◽  
Gene Promoter ◽  
Inhibitory Factor ◽  
Wild Type ◽  
Response Element ◽  
Synergistic Activation ◽  
Pomc Gene ◽  
Wild Type Promoter

We previously have described molecular mechanisms converging at the Nur response element-signal transducer and activator of transcription (STAT) composite site responsible for synergistic activation of the proopiomelanocortin (POMC) gene promoter by leukemia inhibitory factor (LIF) and CRH. In this study, we asked how glucocorticoids (GC), the physiological negative regulators of POMC gene expression, modulate this synergism. In the corticotroph cell line AtT-20, the response of the wild-type promoter to LIF+CRH was barely inhibited by GC, whereas a distal promoter subregion (−414/−293) encompassing the Nur response element-STAT site and devoid of the negative GC-responsive element located in the proximal domain, displayed a cooperative response to LIF + dexamethasone (DEX) and LIF+CRH+DEX treatments. LIF+CRH-stimulated ACTH secretion was also inefficiently inhibited by DEX in the same cell line. This study was focused thereafter on LIF+DEX cooperativity, which may be responsible, on the wild-type promoter, for lack of negative regulation by DEX of the LIF+CRH synergy. The STAT1–3 low-affinity site, in the context of the (−414/−293) subregion of the POMC promoter, was found necessary and sufficient for transcriptional synergism between activated GC receptor (GR) and STAT1–3. Moreover the activities of reporters specific for STAT1–3 or GR were reciprocally enhanced by DEX or LIF. Single and sequential chromatin immunoprecipitations revealed 1) a STAT-dependent corecruitment of coactivators after LIF and LIF+DEX stimulation and 2) a more lasting recruitment of both STAT3 and GR in the same enhanceosome on the endogenous POMC promoter after LIF+DEX joint stimulation than after the single one. Such events may be responsible for a lack of repressive property of GR unmasked on the whole POMC promoter during LIF+CRH stimulation and may contribute to the tonicity of the hypothalamic-pituitary-adrenal axis during inflammatory-infectious diseases.

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