Enrichment of hematopoietic precursor cells and cloning of multipotential B-lymphocyte precursors.

McKearn, John P.; McCubrey, James A.; Fagg, Barbara

doi:10.1073/pnas.82.21.7414

Cited by 152 publications

(118 citation statements)

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“…IL-3 induces colony formation of multiple cell types in cultures of bone marrow or fetal liver cells . It supports the growth and/or differentiation of multipotent precursor cells belonging to both the myeloid and lymphoid lineages as well as more differentiated progenitor cells belonging to the myeloid lineage (2,(11)(12)(13)(14)(15). IL-3 has also been associated with multiple activities and has been termed burstpromoting activity (16), mast cell growth factor (17,18), P cell stimulating factor (19,20), and histamine-producing cell-stimulating factor (21) by various investigators.…”

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confidence: 99%

“…However, the mechanism by which IL-3 mediates these processes is not understood. In this report, we have studied the growth and differentiation of two IL-3-dependent cell lines, FDC-PI (a myeloid progenitor) (22) and FL5 .12 (a lymphoid progenitor) (14) . FDC-P 1 was generated from normal bone marrow cells cultured in the presence of WEHI-3 conditioned medium (CM) and appears to represent a cell early in myelomonocytic differentiation (22) .…”

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confidence: 99%

“…FDC-P 1 was generated from normal bone marrow cells cultured in the presence of WEHI-3 conditioned medium (CM) and appears to represent a cell early in myelomonocytic differentiation (22) . FL5 .12 was generated from the culture of 13-d fetal liver cells in the presence of WEHI-3 CM and represents a multipotential B lymphoid precursor cell since these cells can be induced to generate mature IgM-secreting B cells committed to several different variable region specificities (14) . Both these clones are nonmalignant since they do not form tumors in nude mice .…”

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Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

London

McKearn

1987

The Journal of Experimental Medicine

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Hematopoietic cell development is regulated by a series of growth factors that are progressively restricted in their biological activity. IL-3 is a multi-lineage growth factor that supports the growth and differentiation of progenitor cells belonging to multiple lineages. However, the mechanism by which IL-3 induces proliferation and differentiation of these cells is not completely understood. In this report, we have used two IL-3-dependent cell lines, FDC-P1 (a myeloid progenitor) and F15.12 (a lymphoid progenitor) to investigate IL-3-mediated growth and differentiation. When either FDC-P1 or FL5.12 cells are deprived of IL-3, greater than 90% of all cells accumulate in the G0 phase of the cell cycle. Upon readdition of IL-3, the cells will reenter the active phases of the cell cycle. Therefore, IL-3 can act as both a competence (G0----G1) factor, and a progression (G1----M) factor for hematopoietic precursor clones. FDC-P1 cells can also proliferate in response to granulocyte/macrophage colony-stimulating factor (G/M-CSF) and IL-4 (B cell stimulatory factor 1 [BSF-1]). However, resting (G0) FDC-P1 cells have lost their ability to grow in response to both G/M-CSF and IL-4, even though both factors can induce a G0----G1 transition. Therefore, G/M-CSF or IL-4 behave as progression factors among certain IL-3-responsive clones, and in those cases only in defined points in the cell cycle. Both IL-4 and G/M-CSF can maintain long-term growth of FDC-P1 cells. Upon removal of factor for 24 h, these clones accumulate in the G1 phase of the cell cycle and do not appear to enter G0 even after 36 h of factor deprivation. Therefore, cells maintained in G/M-CSF or IL-4 have altered growth requirements compared with the IL-3-dependent lines from which they were derived. The ability of various hematopoietic growth factors to regulate cell cycle progression in IL-3-dependent cell lines is dependent not only upon the lineage from which these cells were derived, but also the phase of the cell cycle in which those cells reside. The consequences of these interactions dictate the manner by which various clones will respond to CSFs and whether the cells will grow and/or differentiate.

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Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

London

McKearn

1987

The Journal of Experimental Medicine

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“…13,59,61,62,66 The murine IAPLTRs (LS-IAP-LTR, PCI-IAP-LTR, and PCII-IAP-LTR), the MoMuLV-LTR, and the human HTLV-I, HTLV-II, HIV retroviral…”

Section: Nuclear Run-on Transcription Assaysmentioning

confidence: 99%

Differential effects of retroviral long terminal repeats on interleukin-3 gene expression and autocrine transformation

McCubrey

1997

Leukemia

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“…The nontransformed murine fetal liver cell line FL5.12 is dependent on IL-3 for proliferation and survival (42). FL5.12 cells were cultured in FL5.12 medium (RPMI 1640 supplemented with 10% fetal bovine serum, 20 mmol/L HEPES, penicillin/streptomycin, 2 mmol/L L-glutamine, 55 Amol/L h-mercaptoethanol, and 10% supernatant from WEHI-3B cells as a source of IL-3).…”

Section: Cell Lines and Reagentsmentioning

confidence: 99%

Mammalian Target of Rapamycin Promotes Vincristine Resistance through Multiple Mechanisms Independent of Maintained Glycolytic Rate

VanderWeele

Rudin

2005

Molecular Cancer Research

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Deregulation of the phosphoinositide 3-kinase-Akt pathway is a major contributor to oncogenesis and resistance to cancer therapy. Recent work has shown mammalian target of rapamycin (mTOR) to be a major target downstream of Akt that contributes to both transformation and therapeutic resistance. Although inhibitors of Akt are not yet clinically available, rapamycin, a mTOR-specific inhibitor, has long been used as an immunosuppressant, and several rapamycin analogues are now in clinical trials in oncology. Recent data indicate that a mTOR complex phosphorylates Akt, and this complex is insensitive to rapamycin. We show that dominant-negative mTOR diminishes phosphorylation of endogenous Akt and exogenous myristoylated Akt (mAkt), that prolonged exposure to rapamycin also inhibits Akt activation, and that this inhibition is dependent on new protein synthesis. These data suggest that mTOR facilitates Akt activation through mechanisms other than direct phosphorylation. A constitutively active mTOR mutant that fails to enhance Akt phosphorylation nevertheless promotes resistance to multiple antimicrotubule agents, indicating that mTOR also mediates survival independent of Akt. Although Akt-and mTOR-mediated survival has been linked to regulation of cellular metabolism, we also show that survival and metabolic control are separable. The hexokinase inhibitor 5-thioglucose markedly inhibits glycolytic rate but does not diminish vincristine resistance mediated by mAkt or mTOR, and it has only a minor effect on mTOR-or mAkt-mediated resistance to growth factor withdrawal, suggesting that Akt-mTOR-mediated resistance is largely independent of maintenance of glycolytic rate. We conclude that mTOR activity can promote resistance through multiple mechanisms independent of maintained glycolytic rate. (Mol Cancer Res 2005; 3(11):635 -44)

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Enrichment of hematopoietic precursor cells and cloning of multipotential B-lymphocyte precursors.

Cited by 152 publications

References 26 publications

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

Activation and growth of colony-stimulating factor-dependent cell lines is cell cycle stage dependent.

Differential effects of retroviral long terminal repeats on interleukin-3 gene expression and autocrine transformation

Mammalian Target of Rapamycin Promotes Vincristine Resistance through Multiple Mechanisms Independent of Maintained Glycolytic Rate

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