Platelet-derived growth factor receptor/platelet-derived growth factor (PDGFR/PDGF) system is a prognostic and treatment response biomarker with multifarious therapeutic targets in cancers

Appiah-Kubi, Kwaku; Wang, Ying; Qian, Hai; Wu, Min; Yao, Xiaoyuan; Wu, Yan; Chen, Yongchang

doi:10.1007/s13277-016-5069-z

Cited by 49 publications

(30 citation statements)

References 130 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our results show that inhibition of autocrine and paracrine VEGF/ VEGF-R signaling pathway in colorectal cancer cells induced the phenotypes. By contrast, blockade of FGF-R and PDGF-R repressed the phenotypes, consistent with previous reports (15,16).…”

Section: Discussionsupporting

confidence: 92%

“…VEGF-R inhibitors stimulate the expression of genesassociated with invasion and metastasis, such as Snail, Slug, Fak and Axl, leading to local invasion and distant metastasis (20 -22). By contrast, inhibition of FGF-R and PDGF-R expressed on several cancer cells suppresses the evasive phenotypes of them (15,16). These reports support our finding that blockade of tumor cell VEGF-R, but not FGF-R and PDGF-R, accelerated aggressiveness of cancer cells.…”

Section: Discussionsupporting

confidence: 89%

See 1 more Smart Citation

Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor

et al. 2017

View full text Add to dashboard Cite

: Recently, inhibition of tumor angiogenesis has become an important anti-cancer therapy. Tumor angiogenesis is regulated by multiple signaling pathways, including VEGF and VEGF receptor (VEGF-R), FGF and FGF receptor (FGF-R), and PDGF and PDGF receptor (PDGF-R) pathways. Thus, the antiangiogenic agents, such as regorafenib, simultaneously target those receptors on vascular endothelial cells. In addition to endothelial cells, cancer cells express the three receptors, suggesting that the antiangiogenic inhibitors affect tumor cells. In fact, we previously demonstrated that regorafenib directly acted on human colorectal cancer cells and accelerated their apoptosis resistance and migration capability. Thus, we here elucidated how regorafenib induced the malignant phenotypes in colorectal cancer cells. To identify the responsible receptor among the regorafenibtargeting proangiogenic receptors, we examined the effects of a potent selective inhibitor for VEGF-R, FGF-R or PDGF-R on apoptosis resistance and migration capability. We clarified that blockade of VEGF-R, but not FGF-R and PDGF-R, induced the malignant phenotypes. We confirmed that blocking of VEGF ligands derived from colorectal cancer cells also induced the phenotypes. These results suggest that regorafenib progressed the malignancy via prevention of autocrine and paracrine VEGF signaling in colorectal cancer cells.

show abstract

Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 89%

Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor

et al. 2017

View full text Add to dashboard Cite

show abstract

“…CAFs are recruited to the tumor mass by a wide range of soluble factors chronically released by both cancer and inflammatory cells, with platelet-derived growth factor (PDGF)-DD arguably playing a prominent role 22,34 . The PDGF family consists of five dimeric ligands (PDGF-AA, -AB, -BB, -CC, -DD) and two receptor tyrosine kinases (PDGFRα and PDGFRβ), which are predominantly involved in tissue repair and wound healing 35 . Recent studies from our group have shown that, unlike normal cholangiocytes, CCA cells secrete PDGF-DD at high levels, stimulated by the relative hypoxia within the tumor mass.…”

Section: The Tumor Microenvironmentmentioning

confidence: 99%

Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

et al. 2018

View full text Add to dashboard Cite

The acquisition of invasive functions by tumor cells is a first and crucial step towards the development of metastasis, which nowadays represents the main cause of cancer-related death. Cholangiocarcinoma (CCA), a primary liver cancer originating from the biliary epithelium, typically develops intrahepatic or lymph node metastases at early stages, thus preventing the majority of patients from undergoing curative treatments, consistent with their very poor prognosis. As in most carcinomas, CCA cells gradually adopt a motile, mesenchymal-like phenotype, enabling them to cross the basement membrane, detach from the primary tumor, and invade the surrounding stroma. Unfortunately, little is known about the molecular mechanisms that synergistically orchestrate this pro-invasive phenotypic switch. Autocrine and paracrine signals (cyto/chemokines, growth factors, morphogens) permeating the tumor microenvironment undoubtedly play a prominent role in this context. Moreover, a number of recently identified signaling systems are currently drawing attention as putative mechanistic determinants of CCA cell invasion. They encompass transcription factors, protein kinases and phosphatases, ubiquitin ligases, adaptor proteins, and miRNAs, whose aberrant expression may result from either stochastic mutations or the abnormal activation of upstream pro-oncogenic pathways. Herein, we sought to summarize the most relevant molecules in this field, and to discuss their mechanism of action and potential prognostic relevance in CCA. Hopefully, a deeper knowledge of the molecular determinants of CCA invasiveness will help to identify clinically useful biomarkers and novel druggable targets, with the ultimate goal to develop innovative approaches to the management of this devastating malignancy.

show abstract

“…PDGF contributes to the migration, angiogenesis, and proliferation of mesenchymal cells (fibroblasts and smooth muscle cells); it is also thought to contribute to the development of atherosclerosis and fibroproliferative disease 15,16) . VEGF contributes to angiogenesis; however, it also contributes to malignant changes, i.e., the angiogenesis or metastasis of tumors, and is thought to be closely related to the critical worsening of cancer 17,18) .…”

Section: Pdgfmentioning

confidence: 99%

Changes of Vascular Endothelial Growth Factor and Platelet-derived Growth Factor Concentrations in Platelet-rich Plasma After Preparation

Suwa

Nakanishi

Kato-Kogoe

et al. 2017

J. Hard Tissue Biology.

View full text Add to dashboard Cite

Platelet-rich plasma (PRP) is plasma that contains platelets concentrated by centrifugal separation of a blood specimen. Advances in the practical applications of PRP have enabled regenerative therapies for hard tissue. Blood contains many growth factors. Therefore, to more effectively use PRP in the clinical setting, it is important to evaluate how growth factor levels change after PRP preparation. The objective of the present study was to observe how the concentrations of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) in PRP change after preparation. PRPs were prepared from 17 healthy consenting male and female subjects aged 25-32 years. Enzyme-linked immunosorbent assay (ELISA) was used to measure the VEGF and PDGF concentrations at 15, 30, 60, 120 and 1,440 min after PRP preparation. We found that VEGF and PDGF concentrations remained high, and exhibited their highest levels at 24 h after PRP production. This persistence suggests that VEGF and PDGF might remain active in tissue regeneration, even 24 h after PRP is prepared.

show abstract

Platelet-derived growth factor receptor/platelet-derived growth factor (PDGFR/PDGF) system is a prognostic and treatment response biomarker with multifarious therapeutic targets in cancers

Cited by 49 publications

References 130 publications

Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor

Regorafenib induces adaptive resistance of colorectal cancer cells via inhibition of vascular endothelial growth factor receptor

Molecular Mechanisms Driving Cholangiocarcinoma Invasiveness: An Overview

Changes of Vascular Endothelial Growth Factor and Platelet-derived Growth Factor Concentrations in Platelet-rich Plasma After Preparation

Contact Info

Product

Resources

About