Analysis of HPV-Positive and HPV-Negative Head and Neck Squamous Cell Carcinomas and Paired Normal Mucosae Reveals Cyclin D1 Deregulation and Compensatory Effect of Cyclin D2
Status PubMed-not-MEDLINE Jazyk angličtina Země Švýcarsko Médium electronic
Typ dokumentu časopisecké články
Grantová podpora
16-29032A
Agentura Pro Zdravotnický Výzkum České Republiky - International
18-11908S
Grantová Agentura České Republiky - International
Operational Programme Research, Development and Education under the project "Center for Tumor Ecology - Research of the Cancer Microenvironment Supporting Cancer Growth and Spread" (reg. No. CZ.02.1.01/0.0/0.0/16_019/0000785)
Ministerstvo Školství, Mládeže a Tělovýchovy - International
Research and Development for Innovations Operational Program under project no. CZ.1.05/2.1.00/19.0400
Ministerstvo Školství, Mládeže a Tělovýchovy - International
PubMed
32224897
PubMed Central
PMC7226528
DOI
10.3390/cancers12040792
PII: cancers12040792
Knihovny.cz E-zdroje
- Klíčová slova
- 11q13 amplification, CCND1, CCND2, CCND3, D-type cyclins, cell cycle, head and neck squamous cell carcinoma, human papillomavirus, paired tumor-normal samples, patient survival,
- Publikační typ
- časopisecké články MeSH
Aberrant regulation of the cell cycle is a typical feature of all forms of cancer. In head and neck squamous cell carcinoma (HNSCC), it is often associated with the overexpression of cyclin D1 (CCND1). However, it remains unclear how CCND1 expression changes between tumor and normal tissues and whether human papillomavirus (HPV) affects differential CCND1 expression. Here, we evaluated the expression of D-type cyclins in a cohort of 94 HNSCC patients of which 82 were subjected to whole genome expression profiling of primary tumors and paired normal mucosa. Comparative analysis of paired samples showed that CCND1 was upregulated in 18% of HNSCC tumors. Counterintuitively, CCND1 was downregulated in 23% of carcinomas, more frequently in HPV-positive samples. There was no correlation between the change in D-type cyclin expression and patient survival. Intriguingly, among the tumors with downregulated CCND1, one-third showed an increase in cyclin D2 (CCND2) expression. On the other hand, one-third of tumors with upregulated CCND1 showed a decrease in CCND2. Collectively, we have shown that CCND1 was frequently downregulated in HNSCC tumors. Furthermore, regardless of the HPV status, our data suggested that a change in CCND1 expression was alleviated by a compensatory change in CCND2 expression.
Institute of Anatomy 1st Faculty of Medicine Charles University 128 00 Prague Czech Republic
Institute of Microbiology of the Czech Academy of Sciences 142 00 Prague Czech Republic
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