High‐risk human papillomavirus infection in different histological subtypes of renal cell carcinoma

Farhadi, Ali; Behzad-Behbahani, Abbas; Geramizadeh, Bita; Sekawi, Zamberi; Rahsaz, Marjan; Sharifzadeh, Sedigheh

doi:10.1002/jmv.23945

Cited by 28 publications

(27 citation statements)

References 45 publications

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“…Clear cell renal cell carcinoma is the most common histological subtype of renal cell carcinoma, accounting for ~80% of cases of renal tumors (2). Early diagnosis and medical intervention are vital in decreasing mortality rates and promoting quality of life.…”

Section: Introductionmentioning

confidence: 99%

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

Zhang

Kong

2016

Oncology Letters

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Abstract. The regulation of entry into and progression through mitosis is important for cell proliferation. Polo-like kinase 1 (PLK1) is involved in multiple stages of mitosis. Forkhead box protein M1 (FOXM1) has multiple functions in tumorigenesis and, in elevated levels, is frequently associated with cancer progression. The present study reports that FOXM1, a substrate of PLK1, controls the transcription mechanism that mediates the PLK1-dependent regulation of the cell cycle. The present study investigated the expression of PLK1 and FOXM1 in the clear renal cell carcinoma 769-P and ACHN cell lines, and indicated that the expression of PLK1 and FOXM1 are correlated in human renal cell cancer cell lines and that the suppression of PLK1 may decrease the expression of FOXM1. The knockdown of FOXM1 or PLK1 in renal cell cancer cell lines caused cell cycle progression to be blocked. As a result, the present study indicated the involvement of FOXM1 in PLK1-regulated cell cycle progression.

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Section: Introductionmentioning

confidence: 99%

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

Zhang

Kong

2016

Oncology Letters

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“…Other genetic elements, e.g., oncogenes transmitted by cancer-associated viruses, may contribute in DDR and/or cell cycling (11,12). For instance, clinical studies of RCC recently identified presence of DNA from oncogenic human papillomavirus (HPV) 16 or 18 serotypes in 14%–30% of cases (13,14). This should be of interest because HPV oncoproteins may alter DDR and cell cycling (11,12).…”

Section: Introductionmentioning

confidence: 99%

Arsenic trioxide amplifies cisplatin toxicity in human tubular cells transformed by HPV-16 E6/E7 for further therapeutic directions in renal cell carcinoma

et al. 2015

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Human papillomavirus (HPV) DNA integrations may affect therapeutic responses in cancers through ATM network-related DNA damage response (DDR). We studied whether cisplatin-induced DDR was altered in human HK-2 renal tubular cells immortalized by HPV16 E6/E7 genes. Cytotoxicity assays utilized thiazolyl blue dye and DDR was identified by gene expression differences, double-strand DNA breaks, ATM promoter activity, and analysis of cell cycling and side population cells. After cisplatin, HK-2 cells showed greater ATM promoter activity indicating activation of this network, but DDR was muted, since little γH2AX was expressed, DNA strand breaks were absent and cells continued cycling. When HK-2 cells were treated with the MDM2 antagonist inducing p53, nutlin-3, or p53 transcriptional activator, tenovin-1, cell growth decreased but cisplatin toxicity was unaffected. By contrast, arsenic trioxide, which by inhibiting wild-type p53-induced phosphatase-1 that serves responses downstream of p53, and by depolymerizing tubulin, synergistically enhanced cisplatin cytotoxicity including loss of SP cells. Our findings demonstrated that HPV16 E6/E7 altered DDR through p53-mediated cell growth controls, which may be overcome by targeting of WIP1 and other processes, and thus should be relevant for treating renal cell carcinoma.

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“…Microplate hybridization assays were further confirmed by type-specific nested PCR using specific primers to detect HPV16 and HPV18 DNA as described before [20][21][22][23].…”

Section: Type-specific Pcrmentioning

confidence: 99%

A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens

et al. 2019

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Early diagnosis and genotyping of high-risk human papillomavirus (HR-HPV) in cervical tissue specimens is significant for cervical cancer prevention. A sensitive microplate fluorometric hybridization assay (MFHA) was designed for the detection of HPV DNA 16 and 18 in cervical tissue. Following optimization and validation of the method, 60 formalin-fixed and paraffinembedded cervical samples representing different cervical intraepithelial neoplasia grades of HPV-associated lesions were tested to determine the sensitivity and specificity of the assay. Using consensus GP5+/6+ biotin-labeled primers to amplify a conserved region within the L1 gene, the amplicons were added to the microplate wells coated with specific probes for the hybridization of HPV 16 and 18 individually. Final detection was performed with streptavidin-AlexaFluor488 conjugated. The results were then compared with type-specific nested polymerase chain reaction (PCR) and colorimetric microplate assay. While the agreement between the results obtained by the type-specific nested PCR and fluorometric assay for the detection of both HR-HPV types was 100%, this agreement for the detection of HPV type 16 and 18 using microplate colorimetric assay was 94.2% and 85% respectively. Overall, the results of the fluorometric and colorimetric assays are promising for detecting both HR-HPV types in a large number of cervical tissue samples with the higher MFHA assay sensitivity.

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High‐risk human papillomavirus infection in different histological subtypes of renal cell carcinoma

Cited by 28 publications

References 45 publications

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

FOXM1 participates in PLK1-regulated cell cycle progression in renal cell cancer cells

Arsenic trioxide amplifies cisplatin toxicity in human tubular cells transformed by HPV-16 E6/E7 for further therapeutic directions in renal cell carcinoma

A fluorometric hybridization assay for detecting and genotyping high-risk human papillomavirus 16 and 18 in archival tissues of cervical specimens

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