Canine and human sarcomas exhibit predominant FGFR1 expression and impaired viability after inhibition of signaling

2014 ◽  
Vol 54 (9) ◽  
pp. 841-852 ◽  
Author(s):  
Nicole Schweiger ◽  
Marlene Hauck ◽  
Heinrich Steinhoff ◽  
Sandra Sampl ◽  
Martin Reifinger ◽  
...  
Keyword(s):  
Fgfr1 Expression

scholarly journals Clinical association analysis of ependymomas and pilocytic astrocytomas reveals elevated FGFR3 and FGFR1 expression in aggressive ependymomas

BMC Cancer ◽  
2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Birgitta Lehtinen ◽  
Annina Raita ◽  
Juha Kesseli ◽  
Matti Annala ◽  
Kristiina Nordfors ◽  
...  
Keyword(s):  
Association Analysis ◽  
Pilocytic Astrocytomas ◽  
Fgfr1 Expression

scholarly journals FGFR1 Expression and Role in Migration in Low and High Grade Pediatric Gliomas

2019 ◽  
Vol 9 ◽  
Author(s):  
Naomi Egbivwie ◽  
Julia V. Cockle ◽  
Matthew Humphries ◽  
Azzam Ismail ◽  
Filomena Esteves ◽  
...  
Keyword(s):  
High Grade ◽  
Fgfr1 Expression

scholarly journals FGFR1 expression defines clinically distinct subtypes in pancreatic cancer

2018 ◽  
Vol 16 (1) ◽  
Author(s):  
Farhan Haq ◽  
You-Na Sung ◽  
Inkeun Park ◽  
Mahmood Akhtar Kayani ◽  
Faizah Yousuf ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Fgfr1 Expression

scholarly journals Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer

2011 ◽  
Vol 105 (9) ◽  
pp. 1362-1369 ◽  
Author(s):  
K Armstrong ◽  
I Ahmad ◽  
G Kalna ◽  
S S Tan ◽  
J Edwards ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Castrate Resistant Prostate Cancer ◽  
Castrate Resistant ◽  
Fgfr1 Expression

scholarly journals circITGA7 Functions as an Oncogene by Sponging miR-198 and Upregulating FGFR1 Expression in Thyroid Cancer

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Siqi Li ◽  
Junmei Yang ◽  
Xiaoting Liu ◽  
Rui Guo ◽  
Ruidong Zhang
Keyword(s):  
Thyroid Cancer ◽  
Cell Lines ◽  
Circular Rna ◽  
Clinical Findings ◽  
Circular Rnas ◽  
Potential Marker ◽  
And Function ◽  
Functional Analyses ◽  
Fgfr1 Expression

Background. Emerging evidence has indicated that circular RNAs (circRNAs), recognized as functional noncoding transcripts in eukaryotic cells, may be involved in regulating many physiological or pathological processes. However, the regulation and function of circular RNA circITGA7 in thyroid cancer (TC) remains unknown. Methods. In this study, we found that circITGA7 is upregulated in TC cell lines. We then performed functional analyses in the cell lines to support clinical findings. Mechanistically, we demonstrated that circITGA7 can directly bind to miR-198 and reduce the inhibition effect of miR-198 on target FGFR1 expression. Results. We reported an upregulation of circITGA7 in patients with TC. Silencing of circITGA7 inhibits metastasis and proliferation of TC cell lines in vitro. In addition, in the TC cell lines, the knockdown of circITGA7 or overexpression of miR-198 significantly suppressed FGFR1 levels. Mechanistically, we found that circITGA7 acts as miR-198 competitive endogenous RNA (ceRNA) to regulate FGFR1 expression. Conclusions. In summary, circRNA circITGA7 may play a regulatory role in TC and may be a potential marker for TC diagnosis or progression.

scholarly journals Compound deletion of Fgfr3 and Fgfr4 partially rescues the Hyp mouse phenotype

2011 ◽  
Vol 300 (3) ◽  
pp. E508-E517 ◽  
Author(s):  
Hua Li ◽  
Aline Martin ◽  
Valentin David ◽  
L. Darryl Quarles
Keyword(s):  
Phosphate Transport ◽  
Current Data ◽  
Fibroblast Growth ◽  
Wild Type ◽  
Compensatory Response ◽  
Fgf Receptor ◽  
Dihydroxyvitamin D ◽  
1,25 Dihydroxyvitamin D ◽  
Fgfr1 Expression ◽  
Stimulation Of

Uncertainty exists regarding the physiologically relevant fibroblast growth factor (FGF) receptor (FGFR) for FGF23 in the kidney and the precise tubular segments that are targeted by FGF23. Current data suggest that FGF23 targets the FGFR1c-Klotho complex to coordinately regulate phosphate transport and 1,25-dihydroxyvitamin D [1,25(OH)2D] production in the proximal tubule. In studies using the Hyp mouse model, which displays FGF23-mediated hypophosphatemia and aberrant vitamin D, deletion of Fgfr3 or Fgfr4 alone failed to correct the Hyp phenotype. To determine whether FGFR1 is sufficient to mediate the renal effects of FGF23, we deleted Fgfr3 and Fgfr4 in Hyp mice, leaving intact the FGFR1 pathway by transferring compound Fgfr3/Fgfr4-null mice on the Hyp background to create wild-type (WT), Hyp, Fgfr3−/−/Fgfr4−/−, and Hyp/Fgfr3−/−/Fgfr4−/− mice. We found that deletion of Fgfr3 and Fgfr4 in Fgfr3−/−/Fgfr4−/− and Hyp/Fgfr3−/−/Fgfr4−/− mice induced an increase in 1,25(OH)2D. In Hyp/Fgfr3−/−/Fgfr4−/− mice, it partially corrected the hypophosphatemia (Pi = 9.4 ± 0.9, 6.1 ± 0.2, 9.1 ± 0.4, and 8.0 ± 0.5 mg/dl in WT, Hyp, Fgfr3−/−/Fgfr4−/−, and Hyp/Fgfr3−/−/Fgfr4−/− mice, respectively), increased Na-phosphate cotransporter Napi2a and Napi2c and Klotho mRNA expression in the kidney, and markedly increased serum FGF23 levels (107 ± 20, 3,680 ± 284, 167 ± 22, and 18,492 ± 1,547 pg/ml in WT, Hyp, Fgfr3−/−/Fgfr4−/−, and Hyp/Fgfr3−/−/Fgfr4−/− mice, respectively), consistent with a compensatory response to the induction of end-organ resistance. Fgfr1 expression was unchanged in Hyp/Fgfr3−/−/Fgfr4−/− mice and was not sufficient to transduce the full effects of FGF23 in Hyp/Fgfr3−/−/Fgfr4−/− mice. These studies suggest that FGFR1, FGFR3, and FGFR4 act in concert to mediate FGF23 effects on the kidney and that loss of FGFR function leads to feedback stimulation of Fgf23 expression in bone.

scholarly journals Combined FGFR and Akt pathway inhibition abrogates growth of FGFR1 overexpressing EGFR-TKI-resistant NSCLC cells

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Mikkel G. Terp ◽  
Kirstine Jacobsen ◽  
Miguel Angel Molina ◽  
Niki Karachaliou ◽  
Hans C. Beck ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Resistance Mechanisms ◽  
Resistant Cell ◽  
Therapeutic Benefit ◽  
Resistant Cell Line ◽  
Nsclc Patients ◽  
Egfr Tki ◽  
Fgfr1 Expression

AbstractEGFR tyrosine kinase inhibitor (TKI) resistance in non-small cell lung cancer (NSCLC) patients is inevitable. Identification of resistance mechanisms and corresponding targeting strategies can lead to more successful later-line treatment in many patients. Using spectrometry-based proteomics, we identified increased fibroblast growth factor receptor 1 (FGFR1) expression and Akt activation across erlotinib, gefitinib, and osimertinib EGFR-TKI-resistant cell line models. We show that while combined EGFR-TKI and FGFR inhibition showed some efficacy, simultaneous inhibition of FGFR and Akt or PI3K induced superior synergistic growth inhibition of FGFR1-overexpressing EGFR-TKI-resistant NSCLC cells. This effect was confirmed in vivo. Only dual FGFR and Akt inhibition completely blocked the resistance-mediating signaling pathways downstream of Akt. Further, increased FGFR1 expression was associated with significantly lower PFS in EGFR-TKI-treated NSCLC patients, and increased FGFR1 were demonstrated in a few post- vs. pre-EGFR-TKI treatment clinical biopsies. The superior therapeutic benefit of combining FGFR and Akt inhibitors provide the rationale for clinical trials of this strategy.

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