Abstract
Squamous cell carcinomas (SCCs) in the anogenital and head and neck regions are associated with high-risk types of human papillomaviruses (HR-HPV). Deregulation of miRNA expression is an important contributor to carcinogenesis. This study aimed to pinpoint commonly and uniquely deregulated miRNAs in cervical, anal, vulvar, and tonsillar tumors of viral or non-viral etiology, searching for a common set of deregulated miRNAs linked to HPV-induced carcinogenesis. RNA was extracted from tumors and nonmalignant tissues from the same locations. The miRNA expression level was determined by next-generation sequencing. Differential expression of miRNAs was calculated, and the patterns of miRNA deregulation were compared between tumors. The total of deregulated miRNAs varied between tumors of different locations by two orders of magnitude, ranging from 1 to 282. The deregulated miRNA pool was largely tumor-specific. In tumors of the same location, a low proportion of miRNAs were exclusively deregulated and no deregulated miRNA was shared by all four types of HPV-positive tumors. The most significant overlap of deregulated miRNAs was found between tumors which differed in location and HPV status (HPV-positive cervical tumors vs. HPV-negative vulvar tumors). Our results imply that HPV infection does not elicit a conserved miRNA deregulation in SCCs.
Highlights
Human papillomaviruses (HPV), species-specific viruses infecting mucosal and cutaneous epithelium of the host, can cause benign diseases such as papillomata or warts; some HPV types have oncogenic potential and are reported to be responsible for up to 5% of all tumors worldwide and up to 30% of those whose development is attributed to infectious agents [1]
The most common carcinoma associated with HPV infection is cervical cancer, which is caused by HPV in almost 100% of cases
Since deregulation of the cellular miRNA network is commonly observed in carcinogenesis, we aimed to characterize the patterns of miRNA expression in a set of tissue samples encompassing tumors from different anatomical locations and differing in HPV
Summary
Human papillomaviruses (HPV), species-specific viruses infecting mucosal and cutaneous epithelium of the host, can cause benign diseases such as papillomata or warts; some HPV types have oncogenic potential and are reported to be responsible for up to 5% of all tumors worldwide and up to 30% of those whose development is attributed to infectious agents [1]. The most common carcinoma associated with HPV infection is cervical cancer, which is caused by HPV in almost 100% of cases. HPV is associated with other tumors of the anogenital region such as vaginal tumors, where HPV participates in 78% of cases, vulvar tumors with 25% of HPV-positive cases, anal tumors with almost. The second region where HPVs play the etiological role in cancer development is head and neck, especially the oropharyngeal location [3]. The proportion of HPV-associated oropharyngeal cancers is increasing around the world, reaching 40–80% of cases in the USA and 20–90%. The proper molecular profiling of HPV-positive and HPV-negative tumors and comparisons of differences between the two etiologies is necessary for expanding our understanding of the mechanisms of carcinogenesis.
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