Abstract
Cervical cancer, which is significantly associated with high-risk human papillomavirus (HPV) infection, currently ranks the fourth most common cancer among women worldwide. Previous literature reported that the elevated expression of G6PD was significantly correlated with the occurrence and deterioration of human cervical cancer, especially with the cervical cancer with HPV16 and HPV18 infection. In this study, we verified that G6PD expression has a strong positive correlation with HPV16 E6 levels in cervical cancer tissues and cells. In addition, regulating the expression of HPV16 E6 significantly affected the proliferation, apoptosis, migration, and invasion in the cervical cancer HeLa cells, as well as the transcript and protein levels of G6PD. The luciferase reporter assay and ChIP assay proved that HPV16 E6 stimulated the transcription of G6PD mRNA and subsequently enhanced the expression of G6PD through directly binding to the specific sites in the promoter of G6PD. Our findings reveal that HPV16 E6 is a novel regulatory factor of G6PD. Furthermore, by regulating the expression of G6PD, HPV16 E6 might promote the proliferation and migration potential, and inhibit apoptosis of cervical cancer cells, which ultimately contributed to the progression and metastasis of cervical cancer.
Highlights
Cervical cancer is a common cancer in women, which often originates in the lining of the cervix, usually at the junction of the squamous and columnar epithelium [1]
The expression level of HPV16 E6 was positively correlated with the expression levels of Glucose-6-phosphate dehydrogenase (G6PD) in host tumor tissues
The results showed that after HPV16 E6 treatment, the luciferase activity increased by 3.6 times compared to the control group, indicating that HPV16 E6 activated the transcription of G6PD
Summary
Cervical cancer is a common cancer in women, which often originates in the lining of the cervix, usually at the junction of the squamous and columnar epithelium [1]. According to the global survey statistics in 2018, cervical cancer has become the fourth most common cancer among women, and accounts for 7.5% of all female cancer deaths. It is well known that human papillomavirus (HPV), as the most common cause of cervical cancer in women, is a circular nonenveloped double-stranded DNA virus. It is one of the necessary factors for precancerous lesions and invasive cancer of female reproductive tract [4]. According to the statistics from Elaine M Smith and Ana Cecilia Rodrıǵ uez, 70% of all invasive cervical cancer is related to gene types 16 and 18, which account for about 50% of all cervical cancers with HPV infection [5, 6]
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