Aswini R Krishnan1, Avinaash Korrapati2, Angela E Zou3, Yuanhao Qu4, Xiao Qi Wang5, Joseph A Califano6, Jessica Wang-Rodriguez7, Scott M Lippman8, Melbourne F Hovell9, Weg M Ongkeko10. 1. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: arkrishn@ucsd.edu. 2. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: akorrapa@ucsd.edu. 3. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: azou@ucsd.edu. 4. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: yuq024@ucsd.edu. 5. Department of Surgery, The University of Hong Kong, Pokfulam, Hong Kong, China. Electronic address: xqwang@hku.hk. 6. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: jcalifano@ucsd.edu. 7. Veterans Administration Medical Center and Department of Pathology, University of California, San Diego, La Jolla, CA, United States. Electronic address: jessica.wang-rodriguez@va.gov. 8. Department of Medicine and Moores Cancer Center, University of California, San Diego, La Jolla, CA, United States. Electronic address: slippman@ucsd.edu. 9. Graduate School of Public Health, San Diego State University, San Diego, CA, United States. Electronic address: mhovell@cbeachsdsu.org. 10. Department of Otolaryngology-Head and Neck Surgery, University of California, San Diego, La Jolla, CA, United States. Electronic address: wongkeko@ucsd.edu.
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.
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.
Authors: Aswini R Krishnan; Yuanhao Qu; Pin Xue Li; Angela E Zou; Joseph A Califano; Jessica Wang-Rodriguez; Weg M Ongkeko Journal: Oncotarget Date: 2017-12-19
Authors: Johannes Pammer; Heidi Rossiter; Martin Bilban; Leopold Eckhart; Maria Buchberger; Laura Monschein; Michael Mildner Journal: Arch Dermatol Res Date: 2020-03-12 Impact factor: 3.017