Deregulation of E-cadherin by human papillomavirus is not confined to high-risk, cancer-causing types

Leong, Cheng Mee; Doorbar, John; Nindl, Ingo; Yoon, Han-Seung; Hibma, Merilyn

doi:10.1111/j.1365-2133.2010.09968.x

Cited by 26 publications

(21 citation statements)

References 30 publications

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“…In normal skin, E-cadherin adhesion protein mediate the interaction between epidermal keratinocytes and Langerhans cells (LCs), and this interaction is required for the retention of LCs in the skin (32). An aberrant expression of E-cadherin in human papillomavirus infected cervical tissue was associated with a significant reduction in Langerhans cells (33). Considering the role of SP-NK1R interaction in regulating the expression of E-cadherin in corneal epithelial cells (26), the lack of functional NK1R on the ocular surface may cause an aberrant expression of E-cadherin in the corneal epithelium, resulting in a decrease in the number of corneal epithelial DCs as noted in NK1R −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Loss of Neurokinin-1 Receptor Alters Ocular Surface Homeostasis and Promotes an Early Development of Herpes Stromal Keratitis

Gaddipati

Rao

Jerome

et al. 2016

The Journal of Immunology

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Substance P neuropeptide and its receptor neurokinin-1 (NK1R) are reported to present on the ocular surface. In this study, mice lacking functional NK1R exhibited an excessive desquamation of apical corneal epithelial cells in association with an increased epithelial cell proliferation, increased epithelial cell density, but decreased epithelial cell size. The lack of NK1R also resulted in decreased density of corneal nerves, corneal epithelial dendritic cells, and a reduced volume of basal tears. Interestingly, massive accumulation of CD11c+CD11b+ conventional dendritic cells (cDCs) was noted in the bulbar conjunctiva and near the limbal area of corneas from NK1R−/− mice. After ocular HSV-1 infection, the number of cDCs and neutrophils infiltrating the infected corneas was significantly higher in NK1R−/− than C57BL/6J mice. This was associated with an increased viral load in infected corneas of NK1R−/− mice. As a result, the number of IFN-γ secreting virus specific CD4 T cells in the DLNs of NK1R−/− mice was much higher than infected C57BL/6J mice. An increased number of CD4 T cells and mature neutrophils (CD11b+Ly6ghigh) in the inflamed corneas of NK1R−/− mice was associated with an early development of severe HSK. Collectively, our results show that the altered corneal biology of uninfected NK1R−/− mice along with an enhanced immunological response after ocular HSV-1 infection cause an early development of HSK in NK1R−/− mice.

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Section: Discussionmentioning

confidence: 99%

Loss of Neurokinin-1 Receptor Alters Ocular Surface Homeostasis and Promotes an Early Development of Herpes Stromal Keratitis

Gaddipati

Rao

Jerome

et al. 2016

The Journal of Immunology

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“…6,7 This association seems to be independent of the activity of high risk HPV proteins on cell cycle regulators. 8 In many epithelial tumors the escape of cancer cells from the primary tumor is often associated not only with loss of intercellular adhesion but also with concomitant enhanced migratory potential, collectively termed EMT. 9 E-cadherin is the main component of the adhesion molecules that mediate the anchoring of intercellular junctions between keratinocytes.…”

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confidence: 99%

Epithelial-to-Mesenchymal Transition in Penile Squamous Cell Carcinoma

et al. 2015

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“…HPV also inhibits GM-CSF production, preventing LC infiltration into the epithelium 293,294,321 . E- cadherin is reduced in both high and low grade lesions in vivo as well as in vitro organotypic models 154,293,294,296,297,322,323 . High risk E6 and E7 downregulate E-cadherin and do so through several mechanisms 42,151,156,158,296,324,325 .…”

Section: Immune Interactionsmentioning

confidence: 99%

“…High risk E6 and E7 downregulate E-cadherin and do so through several mechanisms 42,151,156,158,296,324,325 . Downregulation of E-cadherin is also seen in lesions caused by low risk HPV types 297 .…”

Section: Immune Interactionsmentioning

confidence: 99%

The Interaction Between Human Papillomaviruses and the Stromal Microenvironment

Woodby

Scott

Bodily

2016

Progress in Molecular Biology and Translational Science

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Human papillomaviruses (HPV) are small, double-stranded DNA viruses that replicate in stratified squamous epithelia and cause a variety of malignancies. Current efforts in HPV biology are focused on understanding the virus-host interactions that enable HPV to persist for years or decades in the tissue. The importance of interactions between tumor cells and the stromal microenvironment has become increasingly apparent in recent years, but how stromal interactions impact the normal, benign life cycle of HPVs or progression of lesions to cancer is less understood. Furthermore, how productively replicating HPV impacts cells in the stromal environment is also unclear. Here we bring together some of the relevant literature on keratinocyte-stromal interactions and their impacts on HPV biology. We discuss how HPV oncogenes in infected cells manipulate other cells in their environment, and, conversely, how neighboring cells may impact the efficiency or course of HPV infection.

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Deregulation of E-cadherin by human papillomavirus is not confined to high-risk, cancer-causing types

Cited by 26 publications

References 30 publications

Loss of Neurokinin-1 Receptor Alters Ocular Surface Homeostasis and Promotes an Early Development of Herpes Stromal Keratitis

Loss of Neurokinin-1 Receptor Alters Ocular Surface Homeostasis and Promotes an Early Development of Herpes Stromal Keratitis

Epithelial-to-Mesenchymal Transition in Penile Squamous Cell Carcinoma

The Interaction Between Human Papillomaviruses and the Stromal Microenvironment

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