Investigation of the influence of high-risk human papillomavirus on the biochemical composition of cervical cancer cells using vibrational spectroscopy

IntroductionPeroxiredoxin 3 (PRX3) is a member of PRX family with antioxidant functions by scavenging hydrogen peroxide. Since the development of cervical cancer is causally linked to high-risk human papillomavirus (HPV) that induces oxidative stress, we conducted the present study to investigate the response of PRX3 to high-risk HPV infection.Material and methodsThis study included fifty-six patients with invasive squamous cervical cancer and sixty control patients with hysteromyoma. Enzyme-linked immunosorbent assay was performed to detect cervical oxidative stress and serum PRX3. The expression of PRX3 and oncoprotein E6 of HPV16 or HPV18 was examined in cervical cancer tissues by immunohistochemistry. Western Blot was applied to detect the expression of PRX3 and E6 in cervical cancer cell lines including CaSki, HeLa, and C33A.ResultsPatients with cervical cancer showed higher serum PRX3 than control patients with hysteromyoma. Levels of oxidative markers in cervical cancer tissues were elevated as compared to normal cervical epithelia. PRX3 expression was upregulated in cervical cancer tissues and the upregulation was positively associated with the expression of E6 of HPV16 or HPV18. The association was confirmed in HPV-containing cervical cancer cell lines including CaSki and HeLa.ConclusionsOur results indicated a positive response of PRX3 to HPV-induced oxidative stress. Serum PRX3 might be a potential indicator of active amplification of high-risk HPV in cervical cancer cells.

Download Full-text

103. High-Capacity Adenoviral Vectors (HCAdV) Armed with a High Risk Human Papillomavirus (HPV) Oncogene Specific CRISPR/Cas9 Machinery Specifically Kill Cervical Cancer Cells

Molecular Therapy ◽

10.1016/s1525-0016(16)32912-4 ◽

2016 ◽

Vol 24 ◽

pp. S44

Author(s):

Eric Ehrke-Schulz ◽

Anja Ehrhardt

Keyword(s):

Cervical Cancer ◽

Human Papillomavirus ◽

High Risk ◽

Cancer Cells ◽

High Capacity ◽

Adenoviral Vectors ◽

Cervical Cancer Cells

Download Full-text

Plasma-based Endogenous Metabolomics Profiling of High-Risk Human Papillomavirus and Their Emerging Roles in the Progression of Cervical Cancer

10.21203/rs.3.rs-914686/v1 ◽

2021 ◽

Author(s):

Qin Wang ◽

Min Xu ◽

Tingting Chen ◽

Jing Chen ◽

Runjie Zhang ◽

...

Keyword(s):

Cervical Cancer ◽

Human Papillomavirus ◽

High Risk ◽

Cancer Cells ◽

Signaling Pathway ◽

Metabolic Phenotype ◽

Cervical Cancer Cells ◽

And Migration ◽

Proliferation And Migration

Abstract Objective: High-risk human papillomavirus (HR-HPV) is the main etiological factor for cervical cancer. Accumulating evidence has suggested that the active role of metabolites in the initiation and progression of cancers. This study was to explore the metabolic profiles of HR-HPV infection and their potential functions in cervical cancer.Methods: Non-targeted metabolomics approach was used to detect metabolic alterations in the plasma obtained from HPV-16 positive (HPV16 (+)), HPV-18 positive (HPV18 (+)) and HPV negative (CTL) individuals, followed by CCK8 experiment to detect the effect of different metabolites on the proliferation of Hela and GH354. A cell migration test then verified significant metabolites on the migration of Hela and GH354. Q RT-qPCR and western blot were used to detect malignant progression related mRNA and protein expression levels of cervical cancer.Results: HR-HPV groups shared 24 dysregulated metabolites (such as amino acids, ceramides, glycerophosphocholines). Further experiments showed ceramide species, including C8 inhibits cervical cancer cells proliferation and migration in vitro. In contrast, C12 significantly enhanced cervical cancer cells proliferation and migration in vitro. Protein and mRNA expressions indicated C8 and C12 were related to the malignant behavior of cervical cancer in vitro. The underlying mechanism demonstrated that C8 intervention inhibited proliferation and migration in cervical cancer cells via the MAPK/JNK signaling pathway, while C12 intervention promoted proliferation and migration in cervical cancer cells via the MAPK/ERK signaling pathway. These findings may contribute to the treatment of HR-HPV-induced cervical cancer by intervening in its initiation and progression.Conclusion: Our study shed some light on how metabolites influenced the relationship between HR-HPV oncogenic capability and metabolic phenotype change and identify species C8 and C12 as critical lipid metabolites that modulate cervical cancer cell’s function.

Download Full-text

Arsenic trioxide inhibits cell proliferation and human papillomavirus oncogene expression in cervical cancer cells

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2014.08.014 ◽

2014 ◽

Vol 451 (4) ◽

pp. 556-561 ◽

Cited By ~ 16

Author(s):

Hongtao Wang ◽

Peng Gao ◽

Jie Zheng

Keyword(s):

Cervical Cancer ◽

Cell Proliferation ◽

Human Papillomavirus ◽

Cancer Cells ◽

Arsenic Trioxide ◽

Oncogene Expression ◽

Cervical Cancer Cells

Download Full-text

Human papillomavirus oncoproteins differentially modulate epithelial-mesenchymal transition in 5-FU-resistant cervical cancer cells

Tumor Biology ◽

10.1007/s13277-016-5143-6 ◽

2016 ◽

Vol 37 (10) ◽

pp. 13137-13154 ◽

Cited By ~ 10

Author(s):

Kanchan Vishnoi ◽

Sutapa Mahata ◽

Abhishek Tyagi ◽

Arvind Pandey ◽

Gaurav Verma ◽

...

Keyword(s):

Cervical Cancer ◽

Human Papillomavirus ◽

Cancer Cells ◽

Epithelial Mesenchymal Transition ◽

Mesenchymal Transition ◽

Cervical Cancer Cells

Download Full-text

Human papillomavirus E5 protein induces expression of the EP4 subtype of prostaglandin E2 receptor in cyclic AMP response element-dependent pathways in cervical cancer cells

Carcinogenesis ◽

10.1093/carcin/bgn236 ◽

2008 ◽

Vol 30 (1) ◽

pp. 141-149 ◽

Cited By ~ 38

Author(s):

Jung-Min Oh ◽

Su-Hyeong Kim ◽

Yun-Il Lee ◽

Miran Seo ◽

So-Young Kim ◽

...

Keyword(s):

Cervical Cancer ◽

Human Papillomavirus ◽

Cyclic Amp ◽

Prostaglandin E2 ◽

Cancer Cells ◽

Response Element ◽

E5 Protein ◽

Cervical Cancer Cells ◽

Cyclic Amp Response Element ◽

Prostaglandin E2 Receptor

Download Full-text

Human Papillomavirus Early Gene Products and Maintenance of the Transformed State of Cervical Cancer Cells in Vitro

Transforming Proteins of DNA Tumor Viruses - Current Topics in Microbiology and Immunology ◽

10.1007/978-3-642-74578-2_21 ◽

1989 ◽

pp. 175-179 ◽

Cited By ~ 2

Author(s):

A. Kleinheinz ◽

M. von Knebel Doeberitz ◽

T. P. Cripe ◽

L. P. Turek ◽

L. Gissmann

Keyword(s):

Cervical Cancer ◽

Human Papillomavirus ◽

Cancer Cells ◽

Early Gene ◽

Gene Products ◽

Cervical Cancer Cells

Download Full-text

Upregulation of miR-205 induces CHN1 expression, which is associated with the aggressive behaviour of cervical cancer cells and correlated with lymph node metastasis

BMC Cancer ◽

10.1186/s12885-020-07478-w ◽

2020 ◽

Vol 20 (1) ◽

Author(s):

Jianbing Liu ◽

Yunfeng Li ◽

Xihua Chen ◽

Xiangbo Xu ◽

Haoqi Zhao ◽

...

Keyword(s):

Cervical Cancer ◽

Lymph Node ◽

High Risk ◽

Cell Growth ◽

Lymph Node Metastasis ◽

Cancer Cells ◽

Migration And Invasion ◽

Node Metastasis ◽

Cervical Cancer Cells ◽

Human Cervical Cancer

Abstract Background Cervical cancer is the leading cause of cancer-related death in women worldwide. However, the mechanisms mediating the development and progression of cervical cancer are unclear. In this study, we aimed to elucidate the roles of microRNAs and a1-chimaerin (CHN1) protein in cervical cancer progression. Methods The expression of miR-205 and CHN1 protein was investigated by in situ hybridisation and immunohistochemistry. We predicted the target genes of miR-205 using software prediction and dual luciferase assays. The expression of mRNAs and proteins was tested by qRT-PCR and western blotting respectively. The ability of cell growth, migration and invasion was evaluated by CCK-8 and transwell. Cell apoptosis was analysed by flow cytometry analysis. Results We found that miR-205 and CHN1 were highly expressed in human cervical cancer tissue compared with paired normal cervical tissues. The CHN1 gene was shown to be targeted by miR-205 in HeLa cells. Interestingly, transfection with miR-205 mimic upregulated CHN1 mRNA and protein, while miR-205 inhibitor downregulated CHN1 in high-risk and human papilloma virus (HPV)-negative human cervical cancer cells in vitro,. These data suggested that miR-205 positively regulated the expression of CHN1. Furthermore, the miR-205 mimic promoted cell growth, apoptosis, migration, and invasion in high-risk and HPV-negative cervical cancer cells, while the miR-205 inhibitor blocked these biological processes. Knockdown of CHN1 obviously reduced the aggressive cellular behaviours induced by upregulation of miR-205, suggesting that miR-205 positively regulated CHN1 to mediate these cell behaviours during the development of cervical cancer. Furthermore, CHN1 was correlated with lymph node metastasis in clinical specimens. Conclusions Our findings showed that miR-205 positively regulated CHN1 to mediate cell growth, apoptosis, migration, and invasion during cervical cancer development, particularly for high-risk HPV-type cervical cancer. These findings suggested that dysregulation of miR-205 and subsequent abnormalities in CHN1 expression promoted the oncogenic potential of human cervical cancer.

Download Full-text