A c-fos/Estrogen Receptor Fusion Protein Promotes Cell Cycle Progression and Proliferation of Human Cancer Cell Lines

Crowe, David L.; Brown, Tamara N.; Kim, Randie H.; Smith, Susan; Lee, Matt K.

doi:10.1006/mcbr.2000.0221

Cited by 22 publications

(18 citation statements)

References 12 publications

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“…Key downstream events include induction of cyclin D2 by c-myc 59 and repression of 2 cyclin-dependent kinase inhibitors (p16 INK4a and p21 Cip1/WAF1 ) that are induced by junB and repressed by c-fos. 60,61 In line with this, transcript levels of c-myb, c-myc, and cyclin D2 were lower whereas those of junB, p16 INK4a , and p21 Cip1/WAF1 were higher in wt LNs compared with thymus DN cells ( Figure 5A,E). However, c-fos levels were not deficient in the wt LNs relative to thymus DN1 cells ( Figure 5A).…”

Section: Wnt and Lif/om Signaling Pathways In Dn Phenotype Cellssupporting

confidence: 65%

T-cell generation by lymph node resident progenitor cells

Terra

Louis

Blanc

et al. 2005

Blood

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IntroductionIn all animals with an adaptive immune system, the thymus is the primary lymphoid organ for T-cell development and no other organ can compensate for defective thymic function. 1 This is problematic considering that progressive thymus atrophy ultimately affects all aging subjects and can even impinge on younger subjects affected by several serious illnesses. [2][3][4] A key question that has baffled immunologists for 40 years is the nature of the signals provided by thymic stromal cells that are necessary and sufficient for T-cell development. 5 Strikingly, recent studies have shown that a bone marrow stromal cell line ectopically expressing the Notch ligand Deltalike-1 (OP9-DL1) acquired the capacity to induce the differentiation of hematopoietic progenitors into functional T cells in vitro. 6,7 A startling and important implication is that the 3-dimensional thymic microenvironment and the presence of thymic epithelial cells are not essential for T-cell development. 6 Thymusindependent T-cell development can also take place in vivo. [8][9][10] Thus, using transgenic mice bearing a green fluorescent protein (GFP) gene placed under the control of the recombinationactivating gene 2 (RAG2) promoter, Guy-Grand et al 9 showed that T lymphopoiesis occurred in lymph nodes (LNs) and less in the Peyer patches of athymic mice. This cryptic T-cell development pathway however generates only limited numbers of mature T cells. 9 Unexpectedly, signals transmitted by the leukemia inhibitory factor (LIF) receptor following prolonged exposure to mouse LIF or bovine oncostatin M (OM) amplify the cryptic LN Tlymphopoietic pathway and transform the mouse LNs into primary T-lymphoid organs. [11][12][13][14][15][16] Thus, about 215 ϫ 10 6 Thy1 ϩ CD4 ϩ CD8 ϩ cells are present in the mesenteric LNs of 12-week-old lckOM transgenic mice that express the OM transgene under the control of the proximal lymphocyte protein tyrosine kinase (lck) promoter. 15 Studies of OM-transgenic mice showed that this extrathymic pathway is thymus independent, generates functional T lymphocytes, and is regulated by a cyclooxygenase-2-dependent proliferation of high endothelial venules. [16][17][18][19] The goal of our work was to determine why LNs are normally unable to support T-cell development and how OM can alleviate this defect. We surmised that such knowledge would provide invaluable information on the essence of a primary T-lymphoid organ, that is, how stromal cells regulate crucial early steps in T-cell development. Materials and methods MiceC57BL/6J (B6) mice were purchased from The Jackson laboratory (Bar Harbor, ME). LckOM transgenic mice on a C57BL/6J background have been previously described. 14,15 From Flow cytometry analysis and cell sortingThe following antibodies were used: biotin and phycoerythrin-cyanin 7 (PE-Cy7) anti-CD8␣ (53-6.7); biotin anti-CD8␤ (53-5.8); allophycocyanin (APC)-Cy7 anti-CD4; biotin anti-NK1.1 (PK136); biotin, APC, and fluorescein isothiocyanate (FITC) anti-T-cell receptor ␤ (anti-TCR␤; H57); biotin anti-TCR...

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Section: Wnt and Lif/om Signaling Pathways In Dn Phenotype Cellssupporting

confidence: 65%

T-cell generation by lymph node resident progenitor cells

Terra

Louis

Blanc

et al. 2005

Blood

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“…Accordingly, FOS knockdown substantially abrogated the capacity of trophoblast cells to proliferate. FOS expression is vital for the proliferative capacity of many cell types in part by regulating the transcriptional activation of cyclin genes and repression of cyclin-dependent kinase inhibitors (52)(53)(54)(55). However, in other cells, FOS seems to be dispensable (56,57) or even down-regulates proliferation (58,59).…”

Section: Discussionmentioning

confidence: 99%

The FOS Transcription Factor Family Differentially Controls Trophoblast Migration and Invasion

Renaud

Kubota

Rumi

et al. 2014

Journal of Biological Chemistry

100

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Background: Trophoblast cells invade the uterus during pregnancy to promote blood flow to the conceptus. Results: The transcription factor FOS inhibits trophoblast invasion, whereas FOS-like (FOSL)-1 promotes invasion. Conclusion:The intracellular balance of FOS family transcription factors modulates trophoblast invasive potential. Significance: Understanding the regulation of trophoblast invasion is crucial for determining the etiology of several placentaassociated obstetrical complications.

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“…Estrogens may protect against colon cancer from direct estrogenic effects on: reduction of bile-acids [60,61]; transcription of estrogen responsive genes, which include several tumor suppressor genes [62,63]; prevention of hypermethylation of the vitamin D [64] and estrogen [65] receptor genes; induction of apoptosis in premalignant cells caused by p53 and p21 protein expression [66]; and reduction of insulin and insulin-like growth factors [67][68][69].…”

Section: Discussionmentioning

confidence: 99%