Protein profiling and identification of modulators regulated by human papillomavirus 16 E7 oncogene in HaCaT keratinocytes by proteomics

Lee, Kyung-Ae; Kang, J S; Shim, Jung‐Hyun; Kho, Chang Won; Park, Sung Goo; Lee, Hee Gu; Paik, Sang‐Gi; Lim, Jong‐Seok; Yoon, Do‐Young

doi:10.1016/j.ygyno.2005.05.039

Cited by 32 publications

(18 citation statements)

References 39 publications

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“…Only a few proteomic studies have been conducted in cervical carcinoma (Bae et al, 2005;Choi et al, 2005;Lee et al, 2005;Lin et al, 2006), for which proteins such as annexin A2, tropomyosin 1 and 2, peroxiredoxin 2 and HSP 27 have been pointed out as potential diagnostic markers.…”

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confidence: 99%

Differential tissue-specific protein markers of vaginal carcinoma

et al. 2009

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The objective was to identify proteins differentially expressed in vaginal cancer to elucidate relevant cancer-related proteins. A total of 16 fresh-frozen tissue biopsies, consisting of 5 biopsies from normal vaginal epithelium, 6 from primary vaginal carcinomas and 5 from primary cervical carcinomas, were analysed using two-dimensional gel electrophoresis (2-DE) and MALDI-TOF mass spectrometry. Of the 43 proteins identified with significant alterations in protein expression between non-tumourous and tumourous tissue, 26 were upregulated and 17 were downregulated. Some were similarly altered in vaginal and cervical carcinoma, including cytoskeletal proteins, tumour suppressor proteins, oncoproteins implicated in apoptosis and proteins in the ubiquitin -proteasome pathway. Three proteins were uniquely altered in vaginal carcinoma (DDX48, erbB3-binding protein and biliverdin reductase) and five in cervical carcinoma (peroxiredoxin 2, annexin A2, sarcomeric tropomyosin kappa, human ribonuclease inhibitor and prolyl-4-hydrolase beta). The identified proteins imply involvement of multiple different cellular pathways in the carcinogenesis of vaginal carcinoma. Similar protein alterations were found between vaginal and cervical carcinoma suggesting common tumourigenesis. However, the expression level of some of these proteins markedly differs among the three tissue specimens indicating that they might be useful molecular markers.

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confidence: 99%

Differential tissue-specific protein markers of vaginal carcinoma

et al. 2009

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“…LEI over-expression slows down this cleavage thus protecting cells from apoptosis suggesting that high expression of LEI in pancreatic carcinoma cells might be jointly responsible for the chemoresistance of human pancreatic cancer. In contrast, studies using papilloma virustransformed keratinocytes indicated a more likely downregulation of LEI (35) obviously reflecting peculiarities of these tumor cells or influence of the microenvironment.…”

Section: Discussionmentioning

confidence: 80%

Nicotinamide phosphoribosyltransferase and prostaglandin H2 synthase 2 are up-regulated in human pancreatic adenocarcinoma cells after stimulation with interleukin-1

Bauer

Venz²,

Junker³

et al. 2009

Int J Oncol

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Abstract. Human pancreatic cancer is today an almost incurable disease with a 5-year survival rate of <5%. Chronic inflammation in the tumor region is often associated with cancer progression. In pancreatic tumors, the pro-inflammatory cytokine IL-1 has been found to affect the development of chemoresistance in this cancer type. In a search for new therapeutic targets we investigated the effect of this proinflammatory mediator on pancreatic cancer protein expression. Therefore, the human pancreatic adenocarcinoma cell line Colo357 was subjected to proteomic analysis after stimulation with IL-1 using 2D gel electrophoresis and mass spectrometry. We detected 11 spots as being differentially expressed after stimulation with IL-1 representing 11 different proteins. Among them, nicotinamide phosphoribosyltransferase (NAMPT) and prostaglandin H 2 synthase 2 (PGHS-2) are crucial proteins whose expression in Colo357 is increased by IL-1. This study is the first one demonstrating an up-regulation of NAMPT in a tumor model for human pancreatic cancer. Several clinical trials using selective PGHS-2 or NAMPT inhibitors alone did not lead to an improvement in clinical outcome. Against the background of a high cardiovascular risk associated with PGHS-2-specific pharmacological inhibitors, we recommend a combinatory treatment with selective NAMPT and PGHS-2 inhibitors. This might overcome the limitations associated with PGHS-2 inhibitors since agents at low doses and with complementary mechanisms will be used. Such combined administration should positively affect the balance between risk and benefit in fighting the interplay of tumor-associated pancreatic inflammation and carcinogenesis in high-risk patients with pancreatic neoplasia. IntroductionPancreatic cancer is the fourth cause of cancer-related mortality in the USA and the sixth one in Europe with more than 250,000 patients estimated to die of the disease worldwide (1). This cancer entity is one of the most deadly of all malignancies with a death to incidence ratio approaching one making mortality rate a robust approximation of incidence for pancreatic cancer (2). The incidence of pancreatic cancer correlates with increasing age reaching a peak in the 65-75-years old age group (3). Approximately three-fourths of patients will die within one year of diagnosis and <5% survive up to 5 years after diagnosis (4). The poor outcome of pancreatic cancer is reflected by non-resectable primary lesions, locally advanced tumors, and a high metastatic potential (5). Since only a few patients benefit from classical adjuvant chemo-and radiotherapy, complete surgical resection is the superior treatment modality for patients with resectable disease. Unfortunately, the majority of pancreatic cancer patients present with locally advanced or metastatic tumors are not amenable for curative surgery. Only a disappointing 15% of patients at the time of diagnosis are eligible to undergo surgical excision, and even patients who have undergone such curative resection often die of recurrent carcin...

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“…These initial findings were further extended by Kyumg-Ae Lee et al, [26]. In this study, HaCaT normal keratinocytes were arranged to stably expressing E7 and an E7-affinity column was used to investigate putative target molecules regulated by E7 expression.…”

Section: Proteomics Studies In Hpv Transformed Cellsmentioning

confidence: 79%

“…Proteomics strategies on HPV-transformed cells Review www.expert-reviews.com Since its introduction 2DE (2D-PAGE) has evolved at different levels becoming the method of choice for differential protein expression analysis in HPV transformed cell extract as well as cervical cancer tissue [25,26]. During isoelectric focusing, proteins are separated using immobilized pH gradient (IPG) strip, while in the second dimension, proteins are separated according to their molecular weight by SDS-PAGE [27].…”

Section: Gel-basedmentioning

confidence: 99%

Proteomics strategies to analyze HPV-transformed cells: relevance to cervical cancer

Domenico

Marco²,

Perluigi

2013

Expert Review of Proteomics

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Cervical cancer is the second most common malignant tumor among women worldwide. The initiating event of cervical cancer is the infection with certain types of human papillomavirus (HPV). Interestingly, viral oncogene expression is necessary but not per se sufficient to promote cervical cancer and other factors are involved in neoplastic progression. Thus, major research efforts should be focused to identify novel co-carcinogenic factors and to understand the mechanisms played into tumor development. To reach this goal, proteomics strategies are powerful tools and a number of studies performed by following this approach have contributed to unravel the interplay between viral infection and protein dysfunction that ultimately results in cancer. The present review summarizes the most relevant findings obtained by applying proteomics technologies to both cell culture models and human tissue specimens. The results suggest that viral oncogenes selectively interact with a subset of intracellular proteins mainly involved in apoptosis resistance, cell growth and differentiation and cell transformation.

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Protein profiling and identification of modulators regulated by human papillomavirus 16 E7 oncogene in HaCaT keratinocytes by proteomics

Cited by 32 publications

References 39 publications

Differential tissue-specific protein markers of vaginal carcinoma

Differential tissue-specific protein markers of vaginal carcinoma

Nicotinamide phosphoribosyltransferase and prostaglandin H2 synthase 2 are up-regulated in human pancreatic adenocarcinoma cells after stimulation with interleukin-1

Proteomics strategies to analyze HPV-transformed cells: relevance to cervical cancer

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