Fibroblast growth factor-2 modulates melanoma adhesion and migration through a syndecan-4-dependent mechanism

Chalkiadaki, Georgia; Nikitovic, Dragana; Berdiaki, Aikaterini; Sifaki, Maria; Krasagakis, Konstantinos; Katonis, Pavlos; Karamanos, Nikos K.; Tzanakakis, George N.

doi:10.1016/j.biocel.2008.11.008

Cited by 62 publications

(55 citation statements)

References 45 publications

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“…M5 epithelioid-like lymph node melanoma cell line (15) and A375 human malignant melanoma cells (ATCC) were maintained in RPMI 1640 medium supplemented with 10% fetal bovine serum (FBS) and gentamycine as previously described (9).…”

Section: Cell Culturesmentioning

confidence: 99%

“…cDNA synthesis was performed using the ThermoScriptTM RT-PCRSystem (Invitrogen, Carlasbad, CA). Real time quantitative PCR was performed using QuantiTech SYBR Green master mix (Qiagen, Valencia, CA) in an Mx3000P cycler as previously described (9). Utilized primers are presented in Table 1.…”

Section: Rna Isolation and Real-time Pcrmentioning

confidence: 99%

“…The cells were treated with heparin (100 lg/ml) for 48 h. Cell extracts were prepared utilizing RIPA buffer (Tris-HCl 50mM, Triton X-100 1%, SDS 0.1%, NaCl 0.15 M, EDTA 1mM, Na 3 VO 4 1%) (9). Cytoplasmic or nuclear proteins were prepared according to Papakonstanti et al (16).…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Importantly, changes in the expression or function of adhesion molecules upgrade melanoma cell migratory capabilities (9) and have been correlated with melanoma progression (10,11). Likewise, the expression of FN, an extracellular matrix component known to affect tumor cell adhesion (12), has been directly connected to aggressive, malignant melanoma progression (13).…”

Section: Introductionmentioning

confidence: 99%

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Heparin plays a key regulatory role via a p53/FAK‐dependent signaling in melanoma cell adhesion and migration

Chalkiadaki¹,

Nikitovic²,

Berdiaki³

et al. 2011

IUBMB Life

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SummaryHeparin and its various derivatives affect cancer progression in humans. In this study, we show that heparin uptaken intracellularly by melanoma cells activated a signaling cascade, which in turn inhibited melanoma cell adhesion and migration. The reduced ability of M5 cells to adhere onto the fibronectin (FN) substrate was directly correlated to a decrease in the expression of focal adhesion kinase (FAK), which is a key regulator of melanoma motility. Cell treatment with heparin caused a marked downregulation in FAK expression (P 0.01). This is followed by an analogous inhibition of both constitutive and FN-induced FAK Y397-phosphorylation (P 0.01). Moreover, heparin stimulated the p53 expression (P 0.001) of M5 cells and its increased accumulation in the nucleus. This favors a decrease in FAK promoter activation and explains the reduced FAK transcript and protein levels. In conclusion, the results of this study clearly demonstrate that the action of heparin in the regulation of melanoma cell adhesion and migration involves a p53/FAK/signaling pathway, which may be of importance in molecular targeted therapy of the disease.

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Section: Cell Culturesmentioning

confidence: 99%

Section: Rna Isolation and Real-time Pcrmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Heparin plays a key regulatory role via a p53/FAK‐dependent signaling in melanoma cell adhesion and migration

Chalkiadaki¹,

Nikitovic²,

Berdiaki³

et al. 2011

IUBMB Life

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“…The utilized ''wound healing assay,'' an established method of assessing cancer cell motility was performed as previously described (14,22). Briefly, MG-63 and Saos 2 cells were seeded in 24-well culture plates at a concentration of 60,000 and 80,000 cells per well, respectively.…”

Section: Wound Healing Assaymentioning

confidence: 99%

Parathyroid hormone (PTH) peptides through the regulation of hyaluronan metabolism affect osteosarcoma cell migration

et al. 2010

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SummaryParathyroid hormone (PTH) strongly stimulates hyaluronan (HA) synthesis and secretion of both normal and carcinogenic cells of the osteoblastic lineage and improves skeletal microarchitecture. HA, a glycosaminoglycan component of the extracellular matrix (ECM), is capable of transmitting ECM-derived signals to regulate cellular function. In this study, we investigated whether the changes of HA metabolism induced by PTH (1-34) and PTH (7-84) peptides in moderately MG-63 and well-differentiated Saos 2 osteosarcoma cell lines, are correlated to their migration capabilities. Our results demonstrate that intermittent PTH (1-34) treatment significantly (P 0.01) supported the migration of MG-63 cells, increased their HA-synthase-2 (HAS2) expression (P 0.001), and enhanced their high-molecular size HA deposition in the pericellular matrix. Both increased endogenous HA production (P 0.01) and treatment with exogenous high-molecular weight HA (P 0.05) correlated to a significant increase of MG-63 cell migration capacity. Transfection with siHAS2 showed that PTH (1-34), mainly through HAS2, enhanced HA and regulated MG-63 cell motility. Interestingly, continuous PTH (1-34) treatment stimulated both Saos 2 cell HAS2 (P 0.001) and HAS1 (P 0.001) isoform expression inhibited their HYAL2 expression (P 0.001) and modestly (P 0.05) enhanced their migration. Therefore, the PTH (1-34) administration mode appears to distinctly modulate the migratory responses of the MG-63 moderately and Saos 2 well-differentiated osteosarcoma cell lines. Conclusively, the obtained data suggest that there is a regulatory effect of PTH (1-34), in an administration mode-dependent manner, on HA metabolism that is essential for osteosarcoma cell migration.

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A reduction in the vascular smooth muscle cell focal adhesion component syndecan‐4 is associated with abdominal aortic aneurysm formation

Wei

et al. 2021

Clinical & Translational Med

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Background Abdominal aortic aneurysm (AAA) is a serious vascular disease for which there is no effective drug treatment. The incidence of AAA increases significantly as a subject ages, and the molecular mechanism of AAA formation remains elusive. In the present study, we investigated the role of syndecan‐4 (SDC4), an important component of focal adhesions, in AAA formation and its association with phenotypic changes in vascular smooth muscle cells (VSMCs). Methods and results The protein expression levels of SDC4 were significantly decreased in human AAA tissue and those of an AAA mouse model. Moreover, SDC4 knockout (KO) in mice accelerated the formation and rupture of AAAs induced by angiotensin II (Ang II) and calcium chloride (CaCl 2 ) Mechanistically, the decrease in SDC4 led to the transformation of cultured VSMCs from a contractile to a secretory phenotype. The RhoA‐F/G‐actin‐myocardin‐related transcription factor‐A (MRTF‐A) signalling pathway was shown to be involved in SDC4‐dependent VSMC alteration. Sphingosine‐1‐phosphate (S1P), a G‐protein‐coupled receptor, attenuated the AAA formation in SDC4‐KO and wild‐type (WT) mice in response to Ang II and CaCl 2 stimulation. Conclusion We herein demonstrated that silencing SDC4 was associated with increased AAA formation and phenotypic changes in VSMCs via the RhoA‐F/G‐actin‐MRTF‐A pathway. These findings indicated that a reduction in SDC4 expression was an important pathological alteration and potential therapeutic target for AAA formation.

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Fibroblast growth factor-2 modulates melanoma adhesion and migration through a syndecan-4-dependent mechanism

Cited by 62 publications

References 45 publications

Heparin plays a key regulatory role via a p53/FAK‐dependent signaling in melanoma cell adhesion and migration

Heparin plays a key regulatory role via a p53/FAK‐dependent signaling in melanoma cell adhesion and migration

Parathyroid hormone (PTH) peptides through the regulation of hyaluronan metabolism affect osteosarcoma cell migration

A reduction in the vascular smooth muscle cell focal adhesion component syndecan‐4 is associated with abdominal aortic aneurysm formation

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