Abstract
High-risk human papillomavirus (HPV) especially HPV-16 and HPV-18 types are speculated to be important risk factors in non-smoking associated lung cancer in Asia. Increasing evidence has demonstrated that HPV oncoproteins may contribute to lung tumorigenesis and cell transformation. Importantly, HPV 16/18 E6 and E7 oncoproteins can mediate expression of multiple target genes and proteins, such as p53/pRb, VEGF, HIF-1α, cIAP-2, and hTERT, and contribute to cell proliferation, angiogenesis and cell immortalization through different signaling pathways in lung cancer. This article provides an overview of experiment data on HPV-associated lung cancer, describes the main targets on which HPV E6/E7 oncoproteins act, and further discusses the potential signaling pathways in which HPV E6/E7 oncoproteins are involved. In addition, we also raise questions regarding existing problems with the study of HPV-associated lung cancer.
Highlights
Human papillomaviruses (HPVs), double-stranded and non-enveloped DNA viruses, belong to the papillomaviridae family
Ikezoe T et al found that non-small cell lung cancer (NSCLC) cells lost their sensitivity to oridonin-induced growth inhibition and apoptosis when p53 was suppressed by over-expression of HPV-16 E6 (Ikezoe et al, 2003)
More studies are needed to explore whether other signaling mediators related to Aryl Hydrocarbon Receptor (AHR) as shown in the gene network are modulated by HPV E6/E7 oncoproteins and subsequently contribute to lung cancer development
Summary
Human papillomaviruses (HPVs), double-stranded and non-enveloped DNA viruses, belong to the papillomaviridae family. A recent meta-analysis suggested that the reported variability in HPV prevalence in lung cancer is better explained by geographical study origin and histological types of cancer than detection method itself (Syrjanen, 2012). This is not a definitive answer to the question. DDX transcription is positively regulated by p53, and p53 inactivated by E6 will lead to the down-regulation of p21 transcription These reports suggest that E6 downregulated p21 through p53-DDX pathway, which would enhance tumor progression in HPV-associated lung cancer (Wu et al, 2011). Ikezoe T et al found that non-small cell lung cancer (NSCLC) cells lost their sensitivity to oridonin-induced growth inhibition and apoptosis when p53 was suppressed by over-expression of HPV-16 E6 (Ikezoe et al, 2003)
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