Human head and neck squamous cell carcinoma cells are both targets and effectors for the angiogenic cytokine, VEGF

Tong, Mingwei; Lloyd, Brandon; Pei, Ping; Mallery, Susan R.

doi:10.1002/jcb.21920

Cited by 29 publications

(35 citation statements)

References 45 publications

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“…33 VEGF up-regulation has been documented in human cutaneous and head and neck SCCs and is hypothesized to play an important role in their pathogenesis. 34,35 Yet another recently proposed hypothesis is that impaired tyrosine kinase signaling may lead to increased dependence on other tumorigenic factors, such as Ras mutation, and that additional Ras blockade may be necessary to treat tumors that are resistant to tyrosine kinase blockade. Ras mutation in human cutaneous SCCs have been reported, but the prevalence of these mutations are low.…”

Section: Discussionmentioning

confidence: 99%

The histologic spectrum of epithelial neoplasms induced by sorafenib

Kwon

Kish

Jaworsky

2009

Journal of the American Academy of Dermatology

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Section: Discussionmentioning

confidence: 99%

The histologic spectrum of epithelial neoplasms induced by sorafenib

Kwon

Kish

Jaworsky

2009

Journal of the American Academy of Dermatology

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“…Previous investigations, by our lab and others, demonstrated that the angiostatic agent, endostatin, inhibited migration and invasion of HNSCC cells, implying that HNSCC cells share some functional characteristics with endothelial cells [8, 9]. In subsequent studies, we demonstrated that HNSCC cells produce exceptionally high levels of VEGF, express both VEGFR1 and VEGFR2, and proliferate in response to autologously produced VEGF [10]. This autocrine-paracrine VEGF growth loop can promote HNSCC tumorigenesis in a biphasic fashion via its proangiogenic and growth promotion roles [10].…”

Section: Introductionmentioning

confidence: 85%

Inherent phenotypic plasticity facilitates progression of head and neck cancer: Endotheliod characteristics enable angiogenesis and invasion

Tong¹,

Han²,

Holpuch³

et al. 2013

Experimental Cell Research

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The presence of the EMT (epithelial-mesenchymal transition), EndMT (endothelial-mesenchymal transition) and VM (vasculogenic mimicry) demonstrates the multidirectional extent of phenotypic plasticity in cancers. Previous findings demonstrating the crosstalk between head and neck squamous cell carcinoma (HNSCC) and vascular endothelial growth factor (VEGF) imply that HNSCC cells share some functional commonalities with endothelial cells. Our current results reveal that cultured HNSCC cells not only possess endothelial-specific markers, but also display endotheliod functional features including low density lipoprotein uptake, formation of tube-like structures on Matrigel and growth state responsiveness to VEGF and endostatin. HNSCC cell subpopulations are also highly responsive to transforming growth factor-β1 and express its auxiliary receptor, endoglin. Furthermore, the endotheliod characteristics observed in vitro recapitulate phenotypic features observed in human HNSCC tumors. Conversely, cultured normal human oral keratinocytes and intact or ulcerated human oral epithelia do not express comparable endotheliod characteristics, which imply that assumption of endotheliod features is restricted to transformed keratinocytes. In addition, this phenotypic state reciprocity facilitates HNSCC progression by increasing production of factors that are concurrently pro-proliferative and pro-angiogenic, conserving cell energy stores by LDL internalization and enhancing cell mobility. Finally, recognition of this endotheliod phenotypic transition provides a solid rationale to evaluate the antitumorigenic potential of therapeutic agents formerly regarded as exclusively angiostatic in scope.

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“…It is prostulated that VEGF targeted therapy has the potential to fulfill both anti-angiogenic and anti-tumorigenic functions (Tong, et al, 2008). As reported, CD44 certainly posseses a valid target for anti-cancer therapy.…”

Section: Associated Targeting Therapymentioning

confidence: 94%