Human Papillomavirus 16 E6 Promotes Angiogenesis of Lung Cancer by SNHG1

Abstract

Human papillomavirus (HPV) is a risk factor for lung cancer. However, the mechanisms underlying is not known. Long noncoding RNAs (lncRNAs) have been found to play an important part in the occurrence and development of lung cancer due to their particular characteristics. HPV induced lung carcinogenesis are incompletely defined. We aim to screen and clarify the functions of lncRNAs that are differentially expressed in HPV related lung cancer. We find that lncRNA SNHG1 is upregulated in lung cancer cells infected with HPV16 E6 by qRT-PCR. Further results demonstrate that SNHG1 overexpression facilitates the tube formation of lung cancer cells in vitro. Our results also indicate that SNHG1 might function in lung cancer by binding with EGFR. Further studies indicate that SNHG1 overexpression can activate nuclear factor κb (NF-κB) pathway which increases the expression of interleukin-6 (IL-6). We also find IL-6 can activate STAT3 pathway which promote the VEGF-D expression. These results expanded our understanding of SNHG1 as a new avenue for therapeutic intervention against lung cancer progression. Upregulation of SNHG1 by HPV infection might be an undefined link between lung cancer and HPV.

No Genetic Causal Association Between Human Papillomavirus and Lung Cancer Risk A Bidirectional Two-Sample Mendelian Randomization Analysis

“…The results of this study contradict some previous reports on the association between HPV infection and lung cancer. A study by NIE Z et al suggests that HPV16 infection may influence the development of lung cancer, particularly by regulating the SNHG1 gene and promoting angiogenesis, which is crucial for tumor growth and spread [47] . A study involving 152 cases of primary lung cancer patients as the lung cancer group and 87 individuals with benign lung lesions as the control group revealed that the incidence of HPV infection in primary lung cancer patients was higher than in those with benign lung lesions.…”