scholarly journals FGF7–FGFR2 autocrine signaling increases growth and chemoresistance of fusion‐positive rhabdomyosarcomas

2021 ◽  
Author(s):  
Christopher I Milton ◽  
Joanna Selfe ◽  
Ewa Aladowicz ◽  
Y.K. Stella Man ◽  
Carolina Bernauer ◽  
...  
Keyword(s):  
Autocrine Signaling

scholarly journals Neuregulin Autocrine Signaling Promotes Self-Renewal of Breast Tumor-Initiating Cells by Triggering HER2/HER3 Activation

2013 ◽  
Vol 74 (1) ◽  
pp. 341-352 ◽  
Author(s):  
Cleo Yi-Fang Lee ◽  
Yuan Lin ◽  
Scott V. Bratman ◽  
Weiguo Feng ◽  
Angera H. Kuo ◽  
...  
Keyword(s):  
Breast Tumor ◽  
Autocrine Signaling ◽  
Tumor Initiating Cells ◽  
Self Renewal

scholarly journals HER2 Overexpression Elicits a Proinflammatory IL-6 Autocrine Signaling Loop That Is Critical for Tumorigenesis

2011 ◽  
Vol 71 (13) ◽  
pp. 4380-4391 ◽  
Author(s):  
Zachary C. Hartman ◽  
Xiao-Yi Yang ◽  
Oliver Glass ◽  
Gangjun Lei ◽  
Takuya Osada ◽  
...  
Keyword(s):  
Her2 Overexpression ◽  
Autocrine Signaling

scholarly journals The first “Slit” is the deepest: the secret to a hollow heart

2008 ◽  
Vol 182 (2) ◽  
pp. 221-223 ◽  
Author(s):  
Iiro Taneli Helenius ◽  
Greg J. Beitel
Keyword(s):  
Cell Shape ◽  
Vascular System ◽  
Hollow Heart ◽  
Autocrine Signaling ◽  
Lumen Formation ◽  
Membrane Surfaces ◽  
Vascular Morphogenesis ◽  
Cell Biol ◽  
Shape Changes

Tubular organs are essential for life, but lumen formation in nonepithelial tissues such as the vascular system or heart is poorly understood. Two studies in this issue (Medioni, C., M. Astier, M. Zmojdzian, K. Jagla, and M. Sémériva. 2008. J. Cell Biol. 182:249–261; Santiago-Martínez, E., N.H. Soplop, R. Patel, and S.G. Kramer. 2008. J. Cell Biol. 182:241–248) reveal unexpected roles for the Slit–Robo signaling system during Drosophila melanogaster heart morphogenesis. In cardioblasts, Slit and Robo modulate the cell shape changes and domains of E-cadherin–based adhesion that drive lumen formation. Furthermore, in contrast to the well-known paracrine role of Slit and Robo in guiding cell migrations, here Slit and Robo may act by autocrine signaling. In addition, the two groups demonstrate that heart lumen formation is even more distinct from typical epithelial tubulogenesis mechanisms because the heart lumen is bounded by membrane surfaces that have basal rather than apical attributes. As the D. melanogaster cardioblasts are thought to have significant evolutionary similarity to vertebrate endothelial and cardiac lineages, these findings are likely to provide insights into mechanisms of vertebrate heart and vascular morphogenesis.

scholarly journals Autocrine signaling by an Aplysia neurotrophin forms a presynaptic positive feedback loop

2018 ◽  
Vol 115 (47) ◽  
pp. E11168-E11177 ◽  
Author(s):  
Iksung Jin ◽  
Hiroshi Udo ◽  
Russell Nicholls ◽  
Huixiang Zhu ◽  
Eric R. Kandel ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Autocrine Signaling ◽  
Positive Feedback Loop ◽  
Short Term Plasticity ◽  
Extracellular Signaling ◽  
Presynaptic Protein ◽  
Long Term Facilitation

Whereas short-term plasticity is often initiated on one side of the synapse, long-term plasticity involves coordinated changes on both sides, implying extracellular signaling. We have investigated the possible signaling role of an Aplysia neurotrophin (ApNT) in facilitation induced by serotonin (5HT) at sensory-to-motor neuron synapses in culture. ApNT is an ortholog of mammalian BDNF, which has been reported to act as either an anterograde, retrograde, or autocrine signal, so that its pre- and postsynaptic sources and targets remain unclear. We now report that ApNT acts as a presynaptic autocrine signal that forms part of a positive feedback loop with ApTrk and PKA. That loop stimulates spontaneous transmitter release, which recruits postsynaptic mechanisms, and presynaptic protein synthesis during the transition from short- to intermediate-term facilitation and may also initiate gene regulation to trigger the transition to long-term facilitation. These results suggest that a presynaptic ApNT feedback loop plays several key roles during consolidation of learning-related synaptic plasticity.

scholarly journals SLAMF7 engagement super-activates macrophages in acute and chronic inflammation

2020 ◽  
Author(s):  
Daimon P. Simmons ◽  
Hung N. Nguyen ◽  
Emma Gomez-Rivas ◽  
Yunju Jeong ◽  
Antonia F. Chen ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Responses ◽  
Inflammatory Cytokine ◽  
Macrophage Activation ◽  
Rna Seq ◽  
Autocrine Signaling ◽  
Tnf Α ◽  
Activated Macrophage ◽  
Ifn Γ ◽  
Acute And Chronic Inflammation

AbstractMacrophages regulate protective immune responses to infectious microbes, but aberrant macrophage activation frequently drives pathological inflammation. To identify regulators of vigorous macrophage activation, we analyzed RNA-seq data from synovial macrophages and identified SLAMF7 as a receptor associated with a super-activated macrophage state in rheumatoid arthritis. We implicated IFN-γ as a key regulator of SLAMF7 expression. Engaging this receptor drove an exuberant wave of inflammatory cytokine expression, and induction of TNF-α following SLAMF7 engagement amplified inflammation through an autocrine signaling loop. We observed SLAMF7-induced gene programs not only in macrophages from rheumatoid arthritis patients, but in gut macrophages from active Crohn’s disease patients and lung macrophages from severe COVID-19 patients. This suggests a central role for SLAMF7 in macrophage super-activation with broad implications in pathology.

scholarly journals DDR1 regulates thyroid cancer cell differentiation via IGF-2/IR-A autocrine signaling loop

2019 ◽  
Vol 26 (1) ◽  
pp. 197-214 ◽  
Author(s):  
Veronica Vella ◽  
Maria Luisa Nicolosi ◽  
Patrizia Cantafio ◽  
Michele Massimino ◽  
Rosamaria Lappano ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Cell Differentiation ◽  
Epithelial To Mesenchymal Transition ◽  
Human Thyroid ◽  
Autocrine Signaling ◽  
Differentiation Markers ◽  
Autocrine Loop ◽  
Mesenchymal Transition ◽  
Poorly Differentiated ◽  
Induced Changes

Patients with thyroid cancers refractory to radioiodine (RAI) treatment show a limited response to various therapeutic options and a low survival rate. The recent use of multikinase inhibitors has also met limited success. An alternative approach relies on drugs that induce cell differentiation, as the ensuing increased expression of the cotransporter for sodium and iodine (NIS) may partially restore sensitivity to radioiodine. The inhibition of the ERK1/2 pathway has shown some efficacy in this context. Aggressive thyroid tumors overexpress the isoform-A of the insulin receptor (IR-A) and its ligand IGF-2; this IGF-2/IR-A loop is associated with de-differentiation and stem-like phenotype, resembling RAI-refractory tumors. Importantly, IR-A has been shown to be positively modulated by the non-integrin collagen receptor DDR1 in human breast cancer. Using undifferentiated human thyroid cancer cells, we now evaluated the effects of DDR1 on IGF-2/IR-A loop and on markers of cell differentiation and stemness. DDR1 silencing or downregulation caused significant reduction of IR-A and IGF-2 expression, and concomitant increased levels of differentiation markers (NIS, Tg, TSH, TPO). Conversely, markers of epithelial-to-mesenchymal transition (Vimentin, Snail-2, Zeb1, Zeb2 and N-Cadherin) and stemness (OCT-4, SOX-2, ABCG2 and Nanog) decreased. These effects were collagen independent. In contrast, overexpression of either DDR1 or its kinase-inactive variant K618A DDR1-induced changes suggestive of less differentiated and stem-like phenotype. Collagen stimulation was uneffective. In conclusion, in poorly differentiated thyroid cancer, DDR1 silencing or downregulation blocks the IGF-2/IR-A autocrine loop and induces cellular differentiation. These results may open novel therapeutic approaches for thyroid cancer.

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