papilloma/protease

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The Impact of Human Papilloma Viruses, Matrix Metallo-Proteinases and HIV Protease Inhibitors on the Onset and Progression of Uterine Cervix Epithelial Tumors: A Review of Preclinical and Clinical Studies.

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Infection of uterine cervix epithelial cells by the Human Papilloma Viruses (HPV) is associated with the development of dysplastic/hyperplastic lesions, termed cervical intraepithelial neoplasia (CIN). CIN lesions may regress, persist or progress to invasive cervical carcinoma (CC), a leading cause

KLK6 protease accelerates skin tumor formation and progression.

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Kallikrein-related peptidase 6 (KLK6) is a serine protease that is aberrantly altered in various types of cancer but its role in non-melanoma skin cancer has not been investigated. KLK6 is active in epidermis and has been linked to normal skin differentiation. Thus, we investigated whether it could

Overexpression of plasminogen activator inhibitor type 2 in basal keratinocytes enhances papilloma formation in transgenic mice.

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The serpin plasminogen activator inhibitor (PAI) type 2 is expressed in differentiated epidermal keratinocytes. To explore its role in this tissue, we studied the impact of PAI-2 overexpression on epidermal differentiation and skin carcinogenesis. A mouse PAI-2-encoding transgene was targeted to

The mRNA coding for the secreted protease transin is expressed more abundantly in malignant than in benign tumors.

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Transin RNA is a 1.9-kilobase RNA transcript induced by oncogenes in rat embryo fibroblast cell lines. We show that RNA species complementary to a cloned transin cDNA are present in mouse skin squamous cell carcinomas induced by a classical initiation-promotion protocol but not in premalignant,

Adjuvant therapy with hydrolytic enzymes in recurrent laryngeal papillomatosis.

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The subject of this study is systemic enzymotherapy as adjuvant treatment in recurrent laryngeal papillomatosis. The authors analyze their observations of 5 adult patients with recurrent laryngeal papillomatosis when after surgical extirpation and subsequent application of peroral proteases there

Raman chemical mapping reveals site of action of HIV protease inhibitors in HPV16 E6 expressing cervical carcinoma cells.

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It has been shown that the HIV protease inhibitors indinavir and lopinavir may have activity against the human papilloma virus (HPV) type 16 inhibiting HPV E6-mediated proteasomal degradation of p53 in cultured cervical carcinoma cells. However, their mode and site of action is unknown. HPV-negative

[Establishment of a SD rat model of vulvar lichen simplex chronicus and detection of the expression of protease activated receptor 2].

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OBJECTIVE To establish a SD rat model of vulvar lichen simplex chronicus (LSC) and investigate the expression of protease activated receptor 2 (PAR2) in the genital skin. METHODS Seventy female SD rats were randomly divided into group A (blank control group, n=10), group B (with application of

[The expression and significance of smac, XIAP, caspase-3 in nonnasal inverted papilloma].

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OBJECTIVE To explore the expression and significance of second mitochondria derived activator of caspase (Smac), X-linked inhibitor of apoptosis protein (XIAP)and cysteine containing aspartate specific protease 3 (caspase-3) in the growth, development and carcinogenesis of the nonnasal inverted

Using HIV drugs to target human papilloma virus.

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Over the past decade it has been demonstrated that HIV protease inhibitors have various off-target activities that has enabled them to be repositioned as treatments for a range of other pathologies. Human papilloma virus and related malignancies have been shown to be susceptible to these agents and

Inhibition of N-nitrosomethylbenzylamine-induced esophageal neoplasms by the Bowman-Birk protease inhibitor.

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Model systems in which carcinogenesis by given agents can be prevented or reduced offer a means of gaining insight into the mechanism(s) of action of carcinogens and the feasibility of chemoprevention in humans. In the current study, the ability of the soy-bean derived Bowman-Birk protease (BBI) to

Specific HIV protease inhibitors inhibit the ability of HPV16 E6 to degrade p53 and selectively kill E6-dependent cervical carcinoma cells in vitro.

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Although HIV protease inhibitor (PI) drugs predominantly target HIV proteases 1 and 2, it is also known that part of their efficacy is due to selective inhibition of the proteasome. The pathogenicity of high-risk human papilloma virus (HPV) is dependent on expression of viral E6 proteins which

E7 protein of human papilloma virus-16 induces degradation of retinoblastoma protein through the ubiquitin-proteasome pathway.

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Rb protein is a critical regulator of entry into the cell cycle, and loss of Rb function by deletions, mutations, or interaction with DNA viral oncoproteins leads to oncogenic transformation. We have shown that the human papilloma virus (HPV)-16 E7 gene is sufficient to induce the immortalization of

Human papillomavirus E7 requires the protease calpain to degrade the retinoblastoma protein.

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Cervical cancers transformed by high risk human papilloma virus (HPV) express the E7 oncoprotein, which accelerates the degradation of the retinoblastoma protein (Rb). Here we show that the E7-mediated degradation of Rb requires the calcium-activated cysteine protease, calpain. E7 bound and

Paracrine communication between malignant and non-malignant prostate epithelial cells in culture alters growth rate, matrix protease secretion and in vitro invasion.

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Epithelial cancer cell invasion is facilitated by stromal cells, immune cells, endothelial cells and other epithelial cells. We have used two human papilloma immortalized prostate cell lines, CA-HPV-10 from a carcinoma and PZ-HPV-7 cells from normal prostatic epithelium to study cell-cell influences

Microenvironmental regulation of the initiated cell.

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In the classical skin model of tumor initiation, keratinocytes treated once with carcinogen retain their normal appearance and growth behavior indefinitely unless promoted to growth into papillomas. Because many of the papillomas regress and may recur with further promotion, their cells can also be

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