Role of Human Papillomavirus Type 16 in Squamous Cell Carcinoma of Upper Aerodigestive Tracts in Colombian Patients

Abstract Background Despite reports of a link between human papillomavirus (HPV) infection and mechanistic target of rapamycin (mTOR) signaling activation, the role of the mTOR pathway, especially raptor and rictor, in HPV-related head and neck cancer is still unclear. The aim of the present study was to elucidate the role of the mTOR pathway in HPV-related oropharyngeal squamous cell carcinoma (OPSCC). Methods The present study involved two strategies. The first was to investigate the activity of mTOR and mTOR-related complexes in high-risk HPV-positive (UM-SCC47 and CaSki) and HPV-negative (SCC-4 and SAS) cancer cell lines. The second was to elucidate mTOR complex expression in 80 oropharyngeal cancer tissues and to examine the relationship between mTOR complex expression and survival in patients with OPSCC. Results The UM-SCC47 and CaSki cell lines showed high gene and protein expression of raptor. They also exhibited G1/S and G2/M phase cell cycle arrest following 24 h incubation with 6 μM temsirolimus, a rapamycin analog, and temsirolimus administration inhibited their growth. HPV-related OPSCC samples showed high gene expression of raptor and rictor compared with HPV-unrelated OPSCC. In addition, HPV-related OPSCC patients with high raptor and rictor expression tended to have a worse prognosis than those with low or medium expression. Conclusions These results suggest that raptor has an important role in HPV-related OPSCC and that temsirolimus is a potential therapeutic agent for patients with HPV-related OPSCC. This is the first report to reveal overexpression of raptor and rictor in HPV-related OPSCC.

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The prognostic role of medical comorbidities in surgically treated human papillomavirus-associated oropharyngeal squamous cell carcinoma

Oral Oncology ◽

10.1016/j.oraloncology.2020.104822 ◽

2020 ◽

Vol 108 ◽

pp. 104822

Author(s):

Linda X. Yin ◽

Cassandra L. Puccinelli ◽

Daniel L. Price ◽

Emily E. Karp ◽

Katharine A. Price ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Human Papillomavirus ◽

Cell Carcinoma ◽

Squamous Cell ◽

Oropharyngeal Squamous Cell Carcinoma ◽

Prognostic Role ◽

Medical Comorbidities

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LncRNA SRA1 is down-regulated in HPV-negative cervical squamous cell carcinoma and regulates cancer cell behaviors

Bioscience Reports ◽

10.1042/bsr20191226 ◽

2019 ◽

Vol 39 (8) ◽

Author(s):

Yunyong Liu ◽

Mengdan Li ◽

Huihui Yu ◽

Haozhe Piao

Keyword(s):

Squamous Cell Carcinoma ◽

Human Papillomavirus ◽

Cell Carcinoma ◽

Cancer Cell ◽

Squamous Cell ◽

Cervical Squamous Cell Carcinoma ◽

Migration And Invasion ◽

Cell Behaviors ◽

Healthy Females

Abstract LncRNA SRA1 plays important roles in several types of human diseases. The present study aimed to explore the role of SRA1 in cervical squamous cell carcinoma (CSCC). In the present study, we showed that plasma SRA1 was down-regulated in human papillomavirus (HPV)-negative CSCC patients but not in HPV-positive CSCC patients compared with healthy females. Down-regulated SRA1 distinguished HPV-negative CSCC patients from HPV-positive CSCC patients and healthy females. In HPV-negative CSCC patients, miR-9 was up-regulated and inversely correlated with SRA1. In HPV-negative CSCC cells, SRA1 overexpression caused the down-regulated miR-9, while miR-9 overexpression failed to affect SRA1. Moreover, SRA1 overexpression caused decreased, while miR-9 overexpression caused increased proliferation, migration and invasion rates of cancer cells. In addition, miR-9 overexpression attenuated the effects of SRA1 overexpression. Therefore, SRA1 is down-regulated in HPV-negative CSCC and regulates cancer cell behaviors possibly by down-regulating miR-9.

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Detection of human papillomavirus type 16 in digital squamous cell carcinoma

The Journal of Dermatology ◽

10.1111/1346-8138.15342 ◽

2020 ◽

Vol 47 (6) ◽

Author(s):

Yuko Kuriyama ◽

Akira Shimizu ◽

Saki Kanai ◽

Jain Kim ◽

Masahito Yasuda ◽

...

Keyword(s):

Squamous Cell Carcinoma ◽

Human Papillomavirus ◽

Cell Carcinoma ◽

Squamous Cell ◽

Human Papillomavirus Type 16

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Expression and Role of E-Cadherin, β-Catenin, and Vimentin in Human Papillomavirus–Positive and Human Papillomavirus–Negative Oropharyngeal Squamous Cell Carcinoma

Journal of Histochemistry & Cytochemistry ◽

10.1369/0022155420950841 ◽

2020 ◽

Vol 68 (9) ◽

pp. 595-606

Author(s):

Hesham Mohamed ◽

Caj Haglund ◽

Lauri Jouhi ◽

Timo Atula ◽

Jaana Hagström ◽

...

Keyword(s):

Stem Cells ◽

Squamous Cell Carcinoma ◽

Human Papillomavirus ◽

Cell Carcinoma ◽

Squamous Cell ◽

Hpv Infection ◽

Vimentin Expression ◽

Regional Metastasis ◽

E Cadherin

Oropharyngeal squamous cell carcinoma (OPSCC) is subclassified by the World Health Organization into two different entities: human papillomavirus (HPV)-positive and HPV-negative tumors. HPV infection promotes the epithelial-to-mesenchymal transition (EMT) and transformation of keratinocyte stem cells into cancer stem cells. EMT is a crucial process in the carcinogenesis of epithelial-derived malignancies, and we aimed to study the role of its markers in OPSCC. This study consists of 202 consecutive OPSCC patients diagnosed and treated with curative intent. We examined E-cadherin, β-catenin, and vimentin expression using immunohistochemistry and compared these with tumor and patient characteristics and treatment outcome. We found that the cell-membranous expression of β-catenin was stronger in HPV-positive than in HPV-negative tumors, and it was stronger in the presence of regional metastasis. The stromal vimentin expression was stronger among HPV-positive tumors. A high E-cadherin expression was associated with tumor grade. No relationship between these markers and survival emerged. In conclusion, β-catenin and vimentin seem to play different roles in OPSCC: the former in the tumor tissue itself, and the latter in the tumor stroma. HPV infection may exploit the β-catenin and vimentin pathways in carcinogenic process. More, β-catenin may serve as a marker for the occurrence of regional metastasis:

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