Clinicopathological significance of fibroblast growth factor 1 in non–small cell lung cancer

Li, Juan; Wei, Zengtao; Li, Hongyu; Dang, Qi; Zhang, Zongpu; Wang, Linlin; Gao, Wei; Zhang, Pei; Yang, Dong; Liu, Jie; Sun, Yehuan

doi:10.1016/j.humpath.2015.07.022

Cited by 24 publications

(14 citation statements)

References 33 publications

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“…In vitro activation of Notch signaling promotes FGF1-mediated cell migration and invasion in HNSCC cell lines As Notch activation was associated with poor patient outcomes in our clinical data and with increased expression of the proinvasive gene FGF1 in vitro, we began our phenotypic characterization by investigating cell migration and invasion as indicators of tumor aggressiveness (28). In vitro cell migration was assessed in control and Notch-a cells using the wound healing (scratch) assay (29).…”

Section: In Vitro Activation Of Notch Signaling Increases Expression mentioning

confidence: 99%

Notch Signaling Activation Is Associated with Patient Mortality and Increased FGF1-Mediated Invasion in Squamous Cell Carcinoma of the Oral Cavity

Weaver

Burch

Cooper

et al. 2016

Molecular Cancer Research

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Section: In Vitro Activation Of Notch Signaling Increases Expression mentioning

confidence: 99%

Notch Signaling Activation Is Associated with Patient Mortality and Increased FGF1-Mediated Invasion in Squamous Cell Carcinoma of the Oral Cavity

Weaver

Burch

Cooper

et al. 2016

Molecular Cancer Research

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“…FGF1 is one of the most important pro‐angiogenic factor involved in tumor angiogenesis . FGF1 is able to regulate angiogenesis independently from VEGF and an enhanced expression of this factor has been reported in different types of tumors . PLAU is a gene that codes for urokinase‐type plasminogen activator (uPA), an enzyme that activates plasmin from plasminogen.…”

Section: Discussionmentioning

confidence: 99%

“…45 FGF1 is able to regulate angiogenesis independently from VEGF 46 and an enhanced expression of this factor has been reported in different types of tumors. 47,48 PLAU is a gene that codes for urokinase-type plasminogen activator (uPA), an enzyme that activates plasmin from plasminogen. Plasmin participates in the proteolytic processes of extracellular matrix degradation which is important for angiogenesis and cancer progression.…”

Section: Discussionmentioning

confidence: 99%

Extracellular vesicles from human liver stem cells inhibit tumor angiogenesis

Lopatina

Grange

Fonsato

et al. 2018

Intl Journal of Cancer

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Human liver stem-like cells (HLSC) and derived extracellular vesicles (EVs) were previously shown to exhibit anti-tumor activity. In our study, we investigated whether HLSC-derived EVs (HLSC-EVs) were able to inhibit tumor angiogenesis in vitro and in vivo, in comparison with EVs derived from mesenchymal stem cells (MSC-EVs). The results obtained indicated that HLSC-EVs, but not MSC-EVs, inhibited the angiogenic properties of tumor-derived endothelial cells (TEC) both in vitro and in vivo in a model of subcutaneous implantation in Matrigel. Treatment of TEC with HLSC-EVs led to the down-regulation of pro-angiogenic genes. Since HLSC-EVs carry a specific set of microRNAs (miRNAs) that could target these genes, we investigated their potential role by transfecting TEC with HLSC-EV specific miRNAs. We observed that four miRNAs, namely miR-15a, miR-181b, miR-320c and miR-874, significantly inhibited the angiogenic properties of TEC in vitro, and decreased the expression of some predicted target genes (ITGB3, FGF1, EPHB4 and PLAU). In parallel, TEC treated with HLSC-EVs significantly enhanced expression of miR-15a, miR-181b, miR-320c and miR-874 associated with the down-regulation of FGF1 and PLAU. In summary, HLSC-EVs possess an anti-tumorigenic effect, based on their ability to inhibit tumor angiogenesis.

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“…ADC accounts for almost 40% of all lung malignancies and its incidence has rapidly increased in recent years [12]. Several targeted drugs against growth factors or their receptor tyrosine kinases have been used to treat ADC [4, 11-13, 28-30]; however, the prognosis of patients remains dismal.…”

Section: Discussionmentioning

confidence: 99%

“…Donnem and colleagues showed that high FGF2 expression in non-small-cell lung cancer (NSCLC) is associated with poor five-year survival [4]. Li demonstrated that immunoreactive scores of FGF1 were higher in NSCLC specimens than in peritumoral normal tissues and patients with high FGF1 expression had a lower overall survival rate [12]. NSCLC patients with high FGF9 expression were also reported to have a worse prognosis than those with low FGF9 expression [13].…”

Section: Introductionmentioning

confidence: 99%

FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma

Song

et al. 2016

Oncotarget

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Several fibroblast growth factor (FGF) isoforms act to stimulate epithelial-mesenchymal transition (EMT) during cancer progression. FGF4 and FGF7 are two ligands of FGF receptor 2 (FGFR2). Using two lung adenocarcinoma (ADC) cell lines, A549 and H1299, we showed that FGF4, but not FGF7, altered cell morphology, promoted EMT-associated protein expression, and enhanced cell proliferation, migration/invasion and colony initiation. In addition, FGF4 increased store-operated calcium entry (SOCE) and expression of the calcium signal-associated protein Orai1. The SOCE inhibitor 2,5-di-tert-butylhydroquinone (BHQ) or Orai1 knockdown reversed all of the EMT-promoting effects of FGF4. BHQ also inhibited FGF4-induced EMT in a mouse xenograft model. Finally, 60 human lung ADC samples and 21 sets of matched specimens (primary and metastatic foci in lymph nodes from one patient) were used to confirm the clinicopathologic significance of FGF4 and its correlation with E-cadherin, Vimentin and Orai1 expression. Our study thus shows that FGF4 induces EMT by elevating SOCE in lung ADC.

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Clinicopathological significance of fibroblast growth factor 1 in non–small cell lung cancer

Cited by 24 publications

References 33 publications

Notch Signaling Activation Is Associated with Patient Mortality and Increased FGF1-Mediated Invasion in Squamous Cell Carcinoma of the Oral Cavity

Notch Signaling Activation Is Associated with Patient Mortality and Increased FGF1-Mediated Invasion in Squamous Cell Carcinoma of the Oral Cavity

Extracellular vesicles from human liver stem cells inhibit tumor angiogenesis

FGF4 induces epithelial-mesenchymal transition by inducing store-operated calcium entry in lung adenocarcinoma

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