Smoking status regulates a novel panel of PIWI-interacting RNAs in head and neck squamous cell carcinoma. (February 2017)

• Record Type: Journal Article
• Authors: Krishnan, Aswini R.; Korrapati, Avinaash; Zou, Angela E.; Qu, Yuanhao; Wang, Xiao Qi; Califano, Joseph A.; Wang-Rodriguez, Jessica; Lippman, Scott M.; Hovell, Melbourne F.; Ongkeko, Weg M.
• Is Part Of: Oral oncology. Volume 65(2017)
• Page Start: 68
• Page End: 75
• Publication Date: 2017-02
• Subjects: Smoking -- Head and neck neoplasms -- RNA -- Small interfering; HNSCC Head and neck squamous cell carcinoma -- ncRNA Noncoding RNA -- piRNA PIWI-interacting RNA; Mouth -- Cancer -- Periodicals; Mouth -- Tumors -- Periodicals; Mouth Diseases -- Periodicals; Mouth Neoplasms -- Periodicals; Bouche -- Cancer -- Périodiques; Bouche -- Tumeurs -- Périodiques; Tumeurs -- Périodiques; Electronic journals; 616.9943105
• DOI: 10.1016/j.oraloncology.2016.12.022
• Languages: English
• ISSNs: 1368-8375

Abstract

Highlights: RNA-seq analysis implicated a 13-member piRNA panel in smoking-related HNSCC. 5 piRNAs correlated with clinical variables, including tumor stage and survival. mRNA expression analysis revealed dysregulation of PIWIL1 in smoking-related HNSCC. 6 piRNAs as well as PIWIL1 associated with common genomic alterations in HNSCC. Abstract: Objective: Smoking remains a primary etiological factor in head and neck squamous cell carcinoma (HNSCC). Given that non-coding RNAs (ncRNAs), including PIWI-interacting RNAs (piRNAs), have emerged as mediators of initiation and progression in head and neck malignancies, we undertook a global study of piRNA expression patterns in smoking-associated HNSCC. Materials and methods: Using RNA-sequencing data from 256 current smoker and lifelong nonsmoker samples in The Cancer Genome Atlas (TCGA), we analyzed the differential expression patterns of 27, 127 piRNAs across patient cohorts stratified by tobacco use, with HPV16 status and tumor status taken into account. We correlated their expression to clinical characteristics and to smoking-induced alterations of PIWI proteins, the functional counterparts of piRNAs. Finally, we correlated our identified piRNAs and PIWI proteins to known chromosomal aberrations in HNSCC to understand their wider-ranging genomic effects. Results and conclusion: Our analyses implicated a 13-member piRNA panel in smoking-related HNSCC, among which NONHSAT123636 and NONHSAT113708 associated with tumor stage, NONHSAT067200 with patient survival, and NONHSAT081250 with smoking-altered PIWIL1 protein expression. 6 piRNAs as well as PIWIL1 correlated with genomic alterations common to HNSCC, including TP53 mutation, TP53-3p co-occurrence, and 3q26, 8q24, and 11q13 amplification. Collectively, our findings provide novel insights into the etiology-specific piRNA landscape of smoking-induced HNSCC.