Cytotoxic effects of docetaxel as a candidate drug of drug-eluting stent on human umbilical vein endothelial cells and the signaling pathway of cell migration inhibition, adhesion delay and shape change

Hu, Tingzhang; Yang, Chun; Fu, Meiling; Yang, Jiali; Du, Rolin; Ran, Xiaolin; Yin, Tieying; Wang, Guixue

doi:10.1093/rb/rbx010

Cited by 22 publications

(17 citation statements)

References 41 publications

(58 reference statements)

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“…Docetaxel or vinorelbine reduced the migration capability of endothelial cells, in agreement with previously reports, describing that both vinorelbine and docetaxel inhibit endothelial cell motility and angiogenesis. In the case of docetaxel, by inhibiting the dynamic instability of www.nature.com/scientificreports www.nature.com/scientificreports/ microtubules that possibly interact with G-proteins associated with focal adhesions and through the VE-cadherin mediated integrin β1/FAK/ROCK signalling pathway [38][39][40] .…”

Section: Discussionmentioning

confidence: 99%

Usefulness of melatonin as complementary to chemotherapeutic agents at different stages of the angiogenic process

González-González

González

Rueda

et al. 2020

Sci Rep

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chemotherapeutics are sometimes administered with drugs, like antiangiogenic compounds, to increase their effectiveness. Melatonin exerts antitumoral actions through antiangiogenic actions. We studied if melatonin regulates the response of HUVECs to chemotherapeutics (docetaxel and vinorelbine). The inhibition that these agents exert on some of the processes involved in angiogenesis, such as, cell proliferation, migratory capacity or vessel formation, was enhanced by melatonin. Regarding to estrogen biosynthesis, melatonin impeded the negative effect of vinorelbine, by decreasing the activity and expression of aromatase and sulfatase. Docetaxel and vinorelbine increased the expression of VEGF-A, VEGF-B, VEGF-C, VEGFR-1, VEGFR-3, ANG1 and/or ANG-2 and melatonin inhibited these actions. Besides, melatonin prevented the positive actions that docetaxel exerts on the expression of other factors related to angiogenesis like JAG1, ANPEP, IGF-1, CXCL6, AKT1, ERK1, ERK2, MMP14 and NOS3 and neutralized the stimulating actions of vinorelbine on the expression of FIGF, FGFR3, CXCL6, CCL2, ERK1, ERK2, AKT1, NOS3 and MMP14. In CAM assay melatonin inhibited new vascularization in combination with chemotherapeutics. Melatonin further enhanced the chemotherapeutics-induced inhibition of p-AKt and p-eRK and neutralized the chemotherapeuticscaused stimulatory effect on HUVECs permeability by modifying the distribution of VE cadherin. Our results confirm that melatonin blocks proangiogenic and potentiates antiangiogenic effects induced by docetaxel and vinorelbine enhancing their antitumor effectiveness.The development of new blood vessels is needed to provide oxygen and nutrients to the tumor cells and a way to escape from the primary site 1 . Angiogenesis is a main step in tumor growth and antiangiogenic agents are considered an interesting complementary strategy in cancer therapy 2 . Angiogenesis is a multi-step process: endothelial cell activation by growth factors, degradation of capillary wall by proteinases, formation of a branch point in the vessel wall, migration of endothelial cells and proliferation and reorganisation of endothelial cells to form tubules. In tumors, the interaction between endothelial cells and the microenvironment stimulates endothelial cells to proliferate, migrate and form a branching network of tubes 3 . A balance between angiogenic activating and inhibiting factors regulates the evolution of endothelial cells from a quiescent to a proangiogenic stage 2 . Among the principal proangiogenic factors are vascular endothelial growth factor (VEGF) and angiopoietins (ANG) 4,5 . Angiogenesis depends on the coordinated balance in time between the production of VEGF and angiopoietins 6 .Melatonin, produced in the pineal gland, has antitumor effects in different cancer types, especially hormone-dependent tumors 7-10 . Melatonin oncostatic actions are exerted through different mechanisms, such as: indirect effects through a down-regulation of gonadal estrogens 11 ; direct antiestrogenic actions at the tumor cell ...

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Section: Discussionmentioning

confidence: 99%

Usefulness of melatonin as complementary to chemotherapeutic agents at different stages of the angiogenic process

González-González

González

Rueda

et al. 2020

Sci Rep

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“…The implantation of DES has a wide range of applications in clinical treatment and has become an effective method for treating cardiovascular diseases [26]. 316L SS is a backbone material of medical cardiovascular stents due to its high ductility, high mechanical strength and good fatigue properties [27, 28].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of in-stent restenosis after graphene oxide double-layer drug coating with good biocompatibility

et al. 2019

Regenerative Biomaterials

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In this study, we designed a double layer-coated vascular stent of 316L stainless steel using an ultrasonic spray system to achieve both antiproliferation and antithrombosis. The coating included an inner layer of graphene oxide (GO) loaded with docetaxel (DTX) and an outer layer of carboxymethyl chitosan (CMC) loaded with heparin (Hep). The coated surface was uniform without aggregation and shedding phenomena before and after stent expanded. The coating treatment was able to inhibit the adhesion and activation of platelets and the proliferation and migration of smooth muscle cells, indicating the excellent biocompatibility and antiproliferation ability. The toxicity tests showed that the GO/DTX and CMC/Hep coating did not cause deformity and organ abnormalities in zebrafish under stereomicroscope. The stents with GO double-layer coating were safe and could effectively prevent thrombosis and in-stent restenosis after the implantation into rabbit carotid arteries for 4–12 weeks.

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“…In addition, docetaxel inhibited the VEGF-induced phosphorylation of focal adhesion kinase, Akt, and eNOS, whose activity is controlled by Hsp90 [129]. Another mechanism involved in docetaxel-mediated inhibition of endothelial cell motility and adhesion involves suppressed VE-cadherin mediated integrin β1/FAK/ROCK signaling pathway [130]. It should also be mentioned that anti-angiogenic activity of docetaxel also extends to its anti-proliferative effect on vascular smooth muscle cells [131].…”

Section: Biology Of Normal Cells Upon Treatment With Platinum Derivatmentioning

confidence: 99%

Comprehensive review on how platinum- and taxane-based chemotherapy of ovarian cancer affects biology of normal cells

Mikuła-Pietrasik

Witucka

Pakuła

et al. 2018

Cell. Mol. Life Sci.

126

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One of the most neglected aspects of chemotherapy are changes, and possible consequences of these changes, that occur in normal somatic cells. In this review, we summarize effects of selected drugs used to treat ovarian cancer (platin derivatives—cisplatin and carboplatin; and taxanes—paclitaxel and docetaxel) on cellular metabolism, acquisition of reactive stroma features, cellular senescence, inflammatory reactions, apoptosis, autophagy, mitophagy, oxidative stress, DNA damage, and angiogenesis in various types of normal cells, including fibroblasts, epithelial cells, endothelial cells, and neurons. The activity of these drugs against the normal cells is presented from a broader perspective of their desirable anti-tumoral effects.

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Cytotoxic effects of docetaxel as a candidate drug of drug-eluting stent on human umbilical vein endothelial cells and the signaling pathway of cell migration inhibition, adhesion delay and shape change

Cited by 22 publications

References 41 publications

Usefulness of melatonin as complementary to chemotherapeutic agents at different stages of the angiogenic process

Usefulness of melatonin as complementary to chemotherapeutic agents at different stages of the angiogenic process

Inhibition of in-stent restenosis after graphene oxide double-layer drug coating with good biocompatibility

Comprehensive review on how platinum- and taxane-based chemotherapy of ovarian cancer affects biology of normal cells

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