Chromosomal integration sites of human papillomavirus DNA in three cervical cancer cell lines mapped by in situ hybridization

1987 ◽  
Vol 176 (5) ◽  
Author(s):  
A. Mincheva ◽  
L. Gissmann ◽  
H. zur Hausen
Keyword(s):  
Cervical Cancer ◽  
In Situ Hybridization ◽  
Human Papillomavirus ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Chromosomal Integration ◽  
Integration Sites ◽  
Papillomavirus Dna

scholarly journals The synergistic therapeutic effect of cisplatin with Human papillomavirus E6/E7 short interfering RNA on cervical cancer cell lines in vitro and in vivo

2011 ◽  
Vol 130 (8) ◽  
pp. 1925-1936 ◽  
Author(s):  
Hun Soon Jung ◽  
Ozgur Cem Erkin ◽  
Mi Jeong Kwon ◽  
Seok Hyung Kim ◽  
Jae In Jung ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Therapeutic Effect ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cervical Cancer Cell ◽  
Short Interfering Rna ◽  
Interfering Rna

scholarly journals Expression of HPV oncogenes from a single integration site in cervical cancer cell lines

2020 ◽  
Author(s):  
Lulu Yu ◽  
Alexei Lobanov ◽  
Vladimir Majerciak ◽  
Sameer Mirza ◽  
Vimla Band ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Lines ◽  
Cancer Cell ◽  
Integration Site ◽  
Cancer Cell Lines ◽  
Virus Genome ◽  
Cervical Cancer Cell ◽  
Dna Integration ◽  
Siha Cells ◽  
Integration Sites

AbstractIntegration of a virus genome into human chromosomal DNA is critical in viral carcinogenesis. In this report, we discovered that virus-host fusion transcripts are characteristically originated mainly from a single integration site in three cervical cancer cell lines, CaSki and SiHa cells with multiple HPV16 DNA integration sites and HeLa cells with multiple HPV18 DNA integration sites. The host genomic elements surrounding the integrated HPV genome are critical for efficient expression of the viral oncogenes. We found that HPV E6 and E7 are expressed by hijacking a host 3’ splice site and/or RNA polyadenylation signal for their production. The viral-host fusion transcripts may encode a chimeric viral-host fusion protein through alternative RNA splicing. One such E6* protein in SiHa cells was found to antagonize E6 function and knockdown of its expression further decreased p53 protein level and increased cell growth by promoting S phase entry. Together, our findings of the integrated virus genome expression only from a given integrated host genomic site will shed new light on possible application of precision medicine and the understanding of HPV carcinogenesis.

Doxycycline inhibits proliferation and induces apoptosis of both human papillomavirus positive and negative cervical cancer cell lines

2016 ◽  
Vol 94 (5) ◽  
pp. 526-533 ◽  
Author(s):  
Yan Zhao ◽  
Xinyu Wang ◽  
Lei Li ◽  
Changzhong Li
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cancer Cell Lines ◽  
Cervical Cancer Cell ◽  
Cervical Cancer Cells

The clinical management of cervical cancer remains a challenge and the development of new treatment strategies merits attention. However, the discovery and development of novel compounds can be a long and labourious process. Drug repositioning may circumvent this process and facilitate the rapid translation of hypothesis-driven science into the clinics. In this work, we show that a FDA-approved antibiotic, doxycycline, effectively targets human papillomavirus (HPV) positive and negative cervical cancer cells in vitro and in vivo. Doxycycline significantly inhibits proliferation of a panel of cervical cancer cell lines. It also induces apoptosis of cervical cancer cells in a time- and dose-dependent manner. In addition, the apoptosis induced by doxycycline is through caspase-dependent pathway. Mechanism studies demonstrate that doxycycline affects oxygen consumption rate, glycolysis, and reduces ATP levels in cervical cancer cells. In HeLa xenograft mouse model, doxycycline significantly inhibits growth of tumour. Our in vitro and in vivo data clearly demonstrate the inhibitory effects of doxycycline on the growth and survival of cervical cancer cells. Our work provides the evidence that doxycycline can be repurposed for the treatment of cervical cancer and targeting energy metabolism may represent a potential therapeutic strategy for cervical cancer.

scholarly journals Biological Activity Characterization of the Diagnostically Relevant Human Papillomavirus 16 E1C RNA

2021 ◽  
Vol 12 (3) ◽  
pp. 539-552
Author(s):  
Christy Susan Varghese ◽  
Rainer Will ◽  
Claudia Tessmer ◽  
Ilse Hofmann ◽  
Bernd Hessling ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Biological Activity ◽  
Human Papillomavirus ◽  
Cell Lines ◽  
Cancer Cell ◽  
Proteasome Inhibition ◽  
Cervical Cancer Cell ◽  
High Grade ◽  
Rna Sequence ◽  
Human Papillomavirus 16

The spliced human papillomavirus 16 (HPV16) E1C RNA is associated with high-grade precursor lesions and cervical cancer. This qualifies E1C as a biomarker for high-grade lesions in HPV-based cervical cancer precursor screening. Here, we aimed to characterize the biological activity of HPV16 E1C RNA. In HEK-293T cells overexpressing HPV16 E1C RNA, we detected 9 kDa E1C protein in the cytoplasm using immunological assays with a newly generated E1C-specific monoclonal antibody or in mass spectrometry only after proteasome inhibition with MG132, indicating instability of the E1C protein. In HPV16-transformed cervical cancer cell lines in which the level of endogenous E1C RNA is much lower, E1C protein was not detected even after proteasome inhibition. Transient E1C overexpression in HEK-293T cells, co-transfected with a firefly luciferase reporter gene under the control of the HPV16 upstream regulatory region (URR), activated the HPV16 URR by 38%. This activation was also present when E1C translation was abolished by mutation. However, a construct expressing a random RNA sequence with similar GC content and 45% homology to the E1C RNA sequence also stimulated URR activity, indicating that special E1C RNA motifs might be responsible for the activation. In HPV16-transformed cell lines W12-episomal (W12-epi), W12-integrated HPV (W12-int), CaSki and SiHa stably overexpressing E1C RNA from lentiviral transduction, levels of endogenous HPV16 RNAs E6*I and E7 remained unchanged, while E1^E4 levels were significantly reduced by 20–30% in W12-epi, W12-int and CaSki cells. Overall, our study shows that E1C RNA is active and might contribute to transformation independent of the E6*I or E7 pathways. However, E1C overexpression resulted in only subtle changes in HPV16 RNA expression and very low copies of endogenous E1C RNA were detected in cervical cancer cell lines. This could weigh towards a less prominent role of E1C RNA in natural HPV transformation.

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