Differential regulation of cell growth and gene expression by FGF-2 and FGF-4 in pituitary lactotroph GH4 cells

Jackson, Twila A.; Koterwas, David M.; Bradford, Andrew P.

doi:10.1016/j.mce.2006.01.002

Cited by 8 publications

(5 citation statements)

References 74 publications

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“…The factors chosen for this study were ideally suited for stem cell expansion in that they were capable of stimulating cell proliferation without differentiation, and have the ability to act as inhibitors of apoptosis [36][37][38][39][40]. This is a key requirement because cells in vitro that are induced to divide or inhibited from differentiation usually undergo apoptosis [41][42][43].…”

Section: Discussionmentioning

confidence: 99%

A Simplified Procedure for Hematopoietic Stem Cell Amplification Using a Serum-Free, Feeder Cell-Free Culture System

Rogers

Yamanaka

Casper

2008

Biology of Blood and Marrow Transplantation

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Umbilical cord blood (UCB) is increasingly being used as a donor source of hematopoietic stem cells (HSCs) to treat blood malignancies. The main limitation to the widespread use of UCB is the low number of HSCs per unit. To compensate, a strategy of in vitro stem cell amplification has been attempted in different research laboratories. The major hurdle blocking success is the creation of culture conditions that support the growth of hematopoietic stem cells without their differentiation. We have designed a simple culture system for stem and progenitor cell expansion that resulted in an increased number of hematopoietic stem cells that maintain their ability to home to the bone marrow and to permanently engraft.

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Section: Discussionmentioning

confidence: 99%

A Simplified Procedure for Hematopoietic Stem Cell Amplification Using a Serum-Free, Feeder Cell-Free Culture System

Rogers

Yamanaka

Casper

2008

Biology of Blood and Marrow Transplantation

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“…In addition, FGF2 can also act as an antiapoptotic factor, rendering tumor cells more resistant to chemotherapy [9]. On the other hand, some researchers have reported that FGF2 can suppress proliferation by a variety of mechanisms, such as apoptosis in chondrocytes [10], p53-independent cell death in Ewing’s sarcoma tumors [11] [12], G1 arrest in MCF-7 human breast cancer cells, rat chondrosarcoma and pituitary lactotroph GH4 cells [13]–[16] and G2 arrest in a human neuroepithelioma cell line [17]. In addition, our laboratory recently reported that exogenous recombinant FGF2 irreversibly inhibits the proliferation of Ras-dependent malignant mouse cells but not immortalized nontumorigenic cell lines [18].…”

Section: Introductionmentioning

confidence: 99%

Fibroblast Growth Factor 2 Causes G2/M Cell Cycle Arrest in Ras-Driven Tumor Cells through a Src-Dependent Pathway

et al. 2013

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We recently reported that paracrine Fibroblast Growth Factor 2 (FGF2) triggers senescence in Ras-driven Y1 and 3T3Ras mouse malignant cell lines. Here, we show that although FGF2 activates mitogenic pathways in these Ras-dependent malignant cells, it can block cell proliferation and cause a G2/M arrest. These cytostatic effects of FGF2 are inhibited by PD173074, an FGF receptor (FGFR) inhibitor. To determine which downstream pathways are induced by FGF2, we tested specific inhibitors targeting mitogen-activated protein kinase (MEK), phosphatidylinositol 3 kinase (PI3K) and protein kinase C (PKC). We show that these classical mitogenic pathways do not mediate the cytostatic activity of FGF2. On the other hand, the inhibition of Src family kinases rescued Ras-dependent malignant cells from the G2/M irreversible arrest induced by FGF2. Taken together, these data indicate a growth factor-sensitive point in G2/M that likely involves FGFR/Ras/Src pathway activation in a MEK, PI3K and PKC independent manner.

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“…Among all of the FGFRs and their different splice variants, bFGF usually activates FGFR2-IIIc (23). Jackson et al (24) found that GH4 rat pituitary cells expressed all four FGFRs, and bFGF phosphorylated the tyrosines of FGFR1, FGFR3 and FGFR4, but not FGFR2, and resulted in no signifi cant change in GH4 cell number, which implys that bioactivity of bFGF on GH4 cell is not mitogenic but regulating neuroendocrine. Background researches have proved that bFGF stimulates PRL, GH and TSH secretion, the effect on PRL being the most prominent (25).…”

Section: Discussionmentioning

confidence: 99%

Basic fibroblast growth factor upregulates expression of growth hormone gene through extracellular signal-regulated kinase 1/2 in GH4 cells

Liu¹,

Luo²,

Chen³

et al. 2013

BLL

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Basic fi broblast growth factor (bFGF) is reported to not only play multifunctions in pituitary differentiation and tumor formation, stimulating cell differentiation or proliferation, also stimulate pituitary to secret prolactin, growth hormone (GH) and thyroid stimulating hormone, although obvious effect on growth hormone only responded to high-dose bFGF. Since it is well documented that both bFGF and GH correlate closely to tumorigenesis, development and metastasis, so it is necessary to reveal the relationship between the cytokines. In the present report we investigated the effect of bFGF on transcription level of GH gene in GH4 rat pituitary cells as well as the regulatory mechanism with real-time reverse transcription polymerase chain reaction and western blotting. We observed a signifi cant expressional increase of GH gene in GH4 cells stimulated by bFGF, meanwhile phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) was also found in the cells. Further investigation unveiled that PD98059, a specifi c inhibitor of ERK1/2 signaling pathway markedly impaired the transcriptional increment of GH gene induced by bFGF in the pituitary cells, which indicates that bFGF upregulates GH gene expression through ERK1/2 signaling pathway in GH4 cells. Results may be helpful to elaborate roles of the two cytokines on tumor (Fig. 3, Ref. 25). Full Text in PDF www.elis.sk.

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Differential regulation of cell growth and gene expression by FGF-2 and FGF-4 in pituitary lactotroph GH4 cells

Cited by 8 publications

References 74 publications

A Simplified Procedure for Hematopoietic Stem Cell Amplification Using a Serum-Free, Feeder Cell-Free Culture System

A Simplified Procedure for Hematopoietic Stem Cell Amplification Using a Serum-Free, Feeder Cell-Free Culture System

Fibroblast Growth Factor 2 Causes G2/M Cell Cycle Arrest in Ras-Driven Tumor Cells through a Src-Dependent Pathway

Basic fibroblast growth factor upregulates expression of growth hormone gene through extracellular signal-regulated kinase 1/2 in GH4 cells

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