Integrated HPV genomes tend to integrate in gene desert areas in the CaSki, HeLa, and SiHa cervical cancer cell lines.
OBJECTIVE
The integration preferences of human papillomavirus (HPV) have been intensively studied and contested over recent years. To disclose the integration preferences of high-risk HPV in cervical cancer, HPV transcriptional sites and features in different cervical cancer cell lines were identified.


METHODS
In this study, three cervical cancer cell lines (CaSki, HeLa, and SiHa) were subjected for HPV genome status determination by amplification of papillomavirus oncogene transcripts (APOT) assay. The numbers of viral copies in human genomes and numbers of viral-human fusion mRNAs in three HPV-integrated cervical cancer cell lines were measured and analysed.


RESULTS
The results revealed that the gene desert region 8q24 of the HPV type 18 integrated HeLa cell line and the 13q21-22 region of the HPV type 16 integrated CaSki and SiHa cell lines were hotspots for HPV integration, and the numbers of viral copies in the human genomes of the three cell lines that we detected were not in accordance with those reported in previous studies.


CONCLUSIONS
Integration of the HPV genome into the host cell chromosome suggests that persistent HPV infection is vital for malignant cell transformation and carcinogenesis. This study provides information to benefit health care professionals seeking more comprehensive and accurate diagnostics for HPV-related disease"? Please check, and amend as necessary.
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing 100052, China; Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Ming-Kun
MK
Diao
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Chu-Yi
CY
Liu
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing 100052, China; Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Hong-Wei
HW
Liu
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing 100052, China; Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China. Electronic address: ljt2000593@163.com.
Jin-Tao
JT
Li
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Fan
F
Li
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Mohammadreza Mohammadzad
MM
Mehryar
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Yang-Junqi
YJ
Wang
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing 100052, China.
Shao-Bing
SB
Zhan
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Yu-Bai
YB
Zhou
Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China.
Ru-Gang
RG
Zhong
National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, and State Key Laboratory for Infectious Disease Prevention and Control, Beijing 100052, China; Beijing Key Laboratory of Environmental and Viral Oncology, College of Life Science and Bio-Engineering, Beijing University of Technology, Beijing 100124, China. Electronic address: zengyicdc1@gmail.com.
Yi
Y
Zeng
D045744:Cell Line, Tumor; D005260:Female; D018628:Gene Dosage; D015967:Gene Expression Regulation, Viral / Q000235:genetics; D016679:Genome, Viral / Q000235:genetics*; D006367:HeLa Cells; D052162:Human papillomavirus 16 / Q000235:genetics*; D052161:Human papillomavirus 18 / Q000235:genetics*; D006801:Humans; D012367:RNA, Viral / Q000235:genetics; D024363:Transcription Initiation Site; D002583:Uterine Cervical Neoplasms / Q000235:genetics*; D016662:Virus Integration / Q000235:genetics*
D012367:RNA, Viral
Cervical cancer; Gene desert areas; Human papillomavirus; Integration