Dual blockade of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF-2) exhibits potent anti-angiogenic effects

Liu, Dong; Xie, Kun; Zhang, Longzhen; Yao, Xiaobo; Li, Hongwen; Xu, Qiaoyu; Wang, Xin; Jiang, Jing; Fang, Jianmin

doi:10.1016/j.canlet.2016.04.036

Cited by 68 publications

(39 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This observation is in line with previous reports that PDGF-CC could up-regulate VEGF production [15]. VEGF was also reported to act as an inducer of indirect action on other angiogenic factors, such as FGF2 and PDGF [36,37]. FGF2 is another considerably important factor that could regulate VEGF expression in ECs and may also play an integral role in resistance to anti-VEGF therapy [38].…”

Section: Cellular Physiology and Biochemistrysupporting

confidence: 81%

Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-α and PDGFR-β

Zhou¹,

Sun²,

Huang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Platelet-derived growth factors (PDGFs) have emerged as pivotal in pathological angiogenesis, which is a hallmark of various tumors and retinal diseases. Here we evaluated the anti-angiogenic effect of imatinib, an inhibitor of PDGF receptors α and β (PDGFR-α and -β), in retinal neovascularization using an oxygen-induced retinopathy (OIR) model. Methods: The OIR model was established and given imatinib or vehicle treatments daily from P12 to P16. At the peak of angiogenesis at P17, the neovascularization area was quantified on retinal whole-mounts with isolectin B4 staining. Immunofluorescence staining and western blots were used to determine the effect of imatinib on different vascular cells and the pathway molecules involved. Results: Imatinib effectively suppressed pathological angiogenesis in OIR mice and reduced the number of all three types of vascular cells, including endothelial cells, pericytes, and smooth muscle cells. Moreover, the expression and activation of PDGFR-α and -β were inhibited by imatinib. The imatinib-treated OIR mice presented with reduced expression of other potent pro-angiogenic factors such as VEGF and FGF2. No obvious retinal or systemic side effects were observed in the imatinib treatment group. Conclusions: Imatinib appears to be safe and effective in suppressing retinal neovascularization. Targeting PDGFs/PDGFRs may also be important for anti-angiogenic treatment and offer a viable alternative treatment for retinal angiogenic diseases.

show abstract

Section: Cellular Physiology and Biochemistrysupporting

confidence: 81%

Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-α and PDGFR-β

Zhou¹,

Sun²,

Huang³

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…A similar requirement for FGF2 in resistance to the multi‐tyrosine kinase inhibitor sunitinib has also been demonstrated (Welti et al, ). In line with this, dual FGF/VEGF inhibitors have shown promising effects in overcoming resistance to VEGF‐targeted therapies in preclinical trials and may present a way to improve anti‐VEGF therapies in the clinic (Li et al, ).…”

Section: Fgf Signaling In the Cancer Environmentmentioning

confidence: 96%

Fibroblast growth factor–mediated crosstalk in cancer etiology and treatment

Clayton

Wilson

Laurent

et al. 2017

Developmental Dynamics

View full text Add to dashboard Cite

It is becoming increasingly evident that multiple cell types within the tumor work together to drive tumour progression and impact on both the response to therapy and the dissemination of tumour cells throughout the body. Fibroblast growth factor signalling (FGF) is perturbed in a number of tumors, serving to drive tumor cell proliferation and migration, but also has a central role in orchestrating the plethora of cells that comprise the tumor microenvironment. This review focuses on how this family of signalling molecules can influence the interactions between tumor cells and their surrounding environment. Unraveling the complexities of FGF signalling between the distinct cell types of a tumor may identify additional opportunities for FGF-targeted compounds in therapy and could help combat drug resistance. Developmental Dynamics 246:493-501, 2017. © 2017 Wiley Periodicals, Inc.

show abstract

“…[34][35][36] Rapamycin inhibited angiogenesis through mTOR pathway in many tumors. [37][38][39] However, a few studies revealed that rapamycin exerted no significant growth inhibition on OSCC cell lines in vitro. 20,21 As a potent survivin inhibitor, YM155 can increase the tumor sensitivity to other anti-cancer agents.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin enhances the anti-angiogenesis and anti-proliferation ability of YM155 in oral squamous cell carcinoma

Wang

Qin

et al. 2017

Tumour Biol.

View full text Add to dashboard Cite

YM155, a small molecule inhibitor of survivin, has been studied in many tumors. It has been shown that YM155 inhibited oral squamous cell carcinoma through promoting apoptosis and autophagy and inhibiting proliferation. It was found that YM155 also inhibited the oral squamous cell carcinoma-mediated angiogenesis through the inactivation of the mammalian target of rapamycin pathway. Rapamycin, a mammalian target of rapamycin inhibitor, played an important role in the proliferation and angiogenesis of oral squamous cell carcinoma cell lines. In our study, cell proliferation assay, transwell assay, tube formation assay, and western blot assay were used to investigate the synergistic effect of rapamycin on YM155 in oral squamous cell carcinoma. Either in vitro or in vivo, rapamycin and YM155 exerted a synergistic effect on the inhibition of survivin and vascular endothelial growth factor through mammalian target of rapamycin pathway. Overall, our results revealed that lowdose rapamycin strongly promoted the sensitivity of oral squamous cell carcinoma cell lines to YM155.

show abstract

Dual blockade of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (FGF-2) exhibits potent anti-angiogenic effects

Cited by 68 publications

References 33 publications

Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-α and PDGFR-β

Imatinib Ameliorated Retinal Neovascularization by Suppressing PDGFR-α and PDGFR-β

Fibroblast growth factor–mediated crosstalk in cancer etiology and treatment

Rapamycin enhances the anti-angiogenesis and anti-proliferation ability of YM155 in oral squamous cell carcinoma

Contact Info

Product

Resources

About