Regulation of HGF and SDF-1 expression by oral fibroblasts – Implications for invasion of oral cancer

Daly, Aisling J.; McIlreavey, Leanne; Irwin, Christopher

doi:10.1016/j.oraloncology.2007.08.012

Cited by 66 publications

(59 citation statements)

References 18 publications

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“…The recruitment of DC stimulated by VLP or LPS was also more important in the presence of HFM. This observation is in agreement with previous studies showing that HFM contain, among other molecules, CXCL12 [30]. All these results suggest that VLP-activated DC have a higher capacity to migrate towards the lymph nodes.…”

Section: Discussionsupporting

confidence: 93%

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

Herman¹,

Hubert²,

Herfs³

et al. 2010

Eur J Immunol

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Human papillomavirus (HPV) infection, particularly type 16, is causally associated with cancer of the uterine cervix. The progression of cervical lesions suggests that viral antigens are not adequately presented to the immune system. The aim of this study was to determine whether HPV16 viral particles can influence the trafficking of human DC/ Langerhans cells (LC), either by direct interactions with DC or following incubation with human normal keratinocytes that are in close contact with LC in the squamous epithelium. We first demonstrated that HPV16 L1 major capsid protein, when self-assembled into virus-like particles (VLP), is able to induce in DC an over-expression of CXC receptor 4 (CXCR4) via the activation of the NF-jB signaling pathway and to enhance DC motility in the presence of CXCL12, suggesting an ability to migrate towards lymph nodes. We also showed that conditioned media of HPV16 VLP-treated keratinocytes induce a lower LC migration than those from untreated keratinocytes and that prostaglandin E2 (PGE 2 ), detected in HPV16 VLP-treated keratinocyte supernatants, may reduce LC recruitment into the squamous epithelium. Taken together, our data demonstrate that HPV16 VLP may differentially regulate the immune protective response according to their target cells.Key words: APC . Cell trafficking . Chemokines . HPV16 VLP Supporting Information available online IntroductionMore than 90% of cervical cancers and precursor lesions (squamous intraepithelial lesions, SIL) may be attributed to the infection by oncogenic types of human papillomavirus (HPV) [1]. However, HPV alone is not sufficient for tumor progression [2]. Additional environmental and/or host factors are probably involved in malignant progression as suggested by the small proportion of infected individuals developing cervical cancer and the relatively long latency period before cancer emergence [3]. The importance of the immune system in the control of HPV infection and lesion development is shown, indirectly, by the high Eur. J. Immunol. 2010. 40: 3075-3084 DOI 10.1002 Immunity to infection 3075 prevalence and persistence of HPV infections in immunosuppressed individuals [4] and by the fact that an increased cellular immune response is correlated with a good clinical prognosis [5]. The DC lineage is a family of professional APC. On exposure to danger signals such as pathogens, immature DC are able to process antigens and to mature through a dramatic change in their cell surface markers [6]. The migration of maturing DC to the draining lymph nodes results in the interactions between DC and naive T cells and in the initiation of an antigen-specific immune response [7]. Furthermore, the signals induced within draining lymph nodes can cause the expansion of lymphatic vessels, sustaining and amplifying the effective homing of DC [8]. Indeed, migration of DC from the site of antigen capture to secondary lymphoid organs is a crucial event in the initiation and amplification of immune responses. In turn, inflammatory sites can recruit circulating...

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Section: Discussionsupporting

confidence: 93%

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

Herman¹,

Hubert²,

Herfs³

et al. 2010

Eur J Immunol

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show abstract

“…For example, SDF-1α supports the proliferation of pre-B lymphocytes in bone marrow stromal cell compartments just as it contributes to proliferation of malignant cells in the primary or secondary tumor. Tumor fibroblasts in breast cancer and OSCC have been shown to secrete SDF-1α, thus supporting the growth of tumor tissue in a paracrine manner (Orimo et al, 2005;Daly et al, 2008). CXCR4 is also expressed on endothelial cells and is critical for normal vascular development of the embryo and also plays a role in tumor angiogenesis by recruiting endothelial cells into the tumor microenvironment.…”

Section: Discussionmentioning

confidence: 99%

CXCL12/SDF‐1α Activates NF‐κB and Promotes Oral Cancer Invasion through the Carma3/Bcl10/Malt1 Complex

Rehman

Wang

2009

Int J Oral Sci

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“…Soluble factors either stem from the cytokine network produced by adjacent stromal cells and act in a paracrine manner, or are released from cells within the group and act in an autocrine or juxtacrine fashion. In oral squamous cell carcinoma in vitro, collective invasion is stimulated by paracrine stromal-cell-derived factor 1 (SDF-1) and hepatocyte growth factor (HGF), which are produced by fibroblasts of the tumor stroma in response to cancer-derived cytokines such as interleukin-1α (IL-1α) (Daly et al, 2008). In sprouting angiogenesis, autocrine regulation of collective endothelial cell sprouting occurs through the secretion of endothelial-cell-derived secreted epidermal growth factor (EGF)-like domain-containing protein 7 (EGFL7), which is deposited into the ECM on the basal side of sprouts and supports outgrowth of nascent vessels .…”

Section: Growth Factors and Chemokinesmentioning

confidence: 99%

Mechanisms of collective cell migration at a glance

Ilina

Friedl

2009

Journal of Cell Science

302

263

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Regulation of HGF and SDF-1 expression by oral fibroblasts – Implications for invasion of oral cancer

Cited by 66 publications

References 18 publications

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

The L1 major capsid protein of HPV16 differentially modulates APC trafficking according to the vaccination or natural infection context

CXCL12/SDF‐1α Activates NF‐κB and Promotes Oral Cancer Invasion through the Carma3/Bcl10/Malt1 Complex

Mechanisms of collective cell migration at a glance

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