Integration of human papillomavirus 18 DNA in esophageal carcinoma 109 cells

Zhang, Ke; Li, Jintao; Li, Shuying; Zhu, Li; Zhou, Ling; Zeng, Yi

doi:10.3748/wjg.v17.i37.4242

Cited by 8 publications

(7 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In a previous study, HPV18 was detected and localized in human chromosome 8 in the esophageal squamous cell carcinoma EC109 cell line, which supported the hypothesis that HPV infection is a pathogenic factor in the development of esophageal cancer (11). Moreover, chronic high-risk HPV infection and the integration of elements of the viral genome into the human chromosome have proven to be pathogenic factors for cervical malignant transformation and lesions (12,13).…”

Section: Introductionsupporting

confidence: 57%

See 1 more Smart Citation

Integration sites of human papillomavirus 18 in esophageal cancer samples

Yan

Sun

et al. 2018

Oncol Lett

Self Cite

View full text Add to dashboard Cite

Abstract. To investigate the association between human papillomavirus (HPV) infection and esophageal cancer, genomic DNA was isolated from 189 samples obtained from patients with esophageal carcinoma, and HPV DNA was identified using the polymerase chain reaction (PCR) with the following specific primers: My09/11 for HPV L1 and HPV18 E6 for HPV18. The HPV18 gene products were sequenced to identify the HPV genotype and the HPV18 integration site was verified using PCR amplification of papillomavirus oncogene transcripts. HPV18 oncogene transcript products were ligated into a pMD-18T plasmid vector and sequenced to confirm the physical location of HPV18 integration. Of the 189 samples, 168 were positive for HPV, of which 33 were positive for HPV18. The sequencing analysis identified two HPV18 E6-positive samples containing one mutation and two samples containing two mutations in the viral DNA. In total ~600 bp of the HPV18 oncogene transcript was detected in three esophageal cancer samples. Sequence analysis revealed that, in two patients, the HPV18 infection was integrated into human chromosome 5, whereas in the remaining sample the virus was integrated into human chromosome 2. The high prevalence of HPV18 infection suggested that HPV18 infection is a pathogenic factor in esophageal carcinoma progression. The integration of HPV18 DNA into the host cell genome suggests that persistent HPV infection has a role in esophageal epithelial cell malignant transformation

show abstract

Section: Introductionsupporting

confidence: 57%

“…Nevertheless, few reports (11)(12)(13)(14) have described the HPV integration site. The objective of the present study was to assess HPV18 infection and its location in the human genome in the setting of EC.…”

Section: Introductionmentioning

confidence: 99%

Integration sites of human papillomavirus 18 in esophageal cancer samples

Yan

Sun

et al. 2018

Oncol Lett

Self Cite

View full text Add to dashboard Cite

show abstract

“…The cell lines, both primary and established, included in the present study were: 2.2.15 [27]; AM-HLH [28]; C4-I, C4-II, CaSki [29]; CU-VI-8 [30]; EC109 [31]; HeLa [29,32]; Hep3B [27,33]; hu-GK14 [34]; HX151c, HX155c, HX156c, HX160c [35]; 37]; Katata [38]; ME-180 [29]; MS1 [39]; MS-B6, MS-T6 [40]; MS751 [29,41] Overall the present analysis identified 628 viral integrants, of which 530.84 (84.53%) were transcriptionally active; in other words, 15.47% of the integrants were silent. One study regarding HHV-4 reported that 90-92% of the integrants in the screened cells were active [36]; the higher level was used herein to report the proportion of active viral centers, hence the fractional number.…”

Section: Resultsmentioning

confidence: 99%

“…The cell lines, both primary and established, included in the present study were: 2.2.15 [27]; AM-HLH [28]; C4-I, C4-II, CaSki [29]; CU-VI-8 [30]; EC109 [31]; HeLa [29,32]; Hep3B [27,33]; hu-GK14 [34]; HX151c, HX155c, HX156c, HX160c [35]; IB-4 [36,37]; Katata [38]; ME-180 [29]; MS1 [39]; MS-B6, MS-T6 [40]; MS751 [29,41]; NAB-2 [42]; Namalwa-C18 [36]; Pal-1 [43]; PCL/PRF/5 [27]; QG-U, QG-H [44]; SiHa [29,45]; SKG-I, SKG-II, SKG-III [44]; SNU-182, SNU-354, SNU-368, SNU-387, SNU-398, SNU-423, SNU-449, SNU 475 [46]; SNU-739, SNU-761, SNU-878, SNU-886 [47]; UM-SCV-6 [48]; UD-SCC-2, UD-SCC-047 [49]; UPCI:SCC090 [50]; and UPCI:SCC154 [49]. Overall the present analysis identified 628 viral integrants, of which 530.84 (84.53%) were transcriptionally active; in other words, 15.47% of the integrants were silent.…”

Section: Resultsmentioning

confidence: 99%

Proportion of Transcriptionally Active Dna Virus Integrants: A Meta-Analysis

Marongiu

2017

Future Virol.

View full text Add to dashboard Cite

Oncoviruses are collectively responsible for over 1,000,000 new cases of cancer per year; some can integrate into the host's chromosomes. The present work was aimed at assessing the proportion of transcriptionally active viral integrants through a systematic review of the scientific publications present on the MedLine database. From the articles screened, 628 viral integrants overall were retrieved, of which 530.84 were transcriptionally active (84.53%); among the clinical samples, 264 of 323 integrants were active (81.73%). The causes for the silencing were not addressed in the articles analyzed. These findings might highlight a possible risk factor for the insurgence of cancer since some oncovirus integrants could be reactivated by stimuli of disparate nature. Further studies should address such possibility. About 16% of all cancer cases have been identified having an infectious aetiology [1]. Hepatitis B virus (HBV), human papilloma virus (HPV), human herpes 4 virus (HHV-4, historically known as Epstein-Barr virus [EBV]) and human herpes 8 virus (HHV-8, previously Kaposi sarcoma herpes virus) are collectively responsible for 56.2% of the incident microbial-related cancer cases, corresponding to over 1,200,000 new cases per year [2].HBV, HPV and HHV-4 share the capability of integrating into the host's chromosomes whereas HHV-8 integrants have not been observed [3]. In addition, other DNA viruses with transformation potential can integrate: Merkel cell polyomavirus (MCPV), human herpes 6 virus (HHV-6) and, in a lesser extent, adenovirus (AdV) [4][5][6]. The infection with these viruses is associated with a wide range of cancer types: HBV with hepatocarcinoma; HPV with virtually all cases of cervical cancer and in a significant proportion of other tumors, for instance in the head and neck; HHV-4 with a number of malignancies, in particular Burkitt and Hodgkin lymphomas, in both immunologically deficient and competent patients; HHV-8 DNA has been retrieved in all Kaposi sarcoma lesions even in immunocompetent hosts; MCPV is recognized as the causative agent of the Merkel cell carcinoma; HHV-6 has been involved in lymphoproliferative diseases; and AdV has been shown to transform rodent cells [1,[7][8][9].All these viruses encode for proteins that disrupt the cell cycle and DNA damage repair response to sustain the viral replication. For example, HBV X, HPV E6/E7, HHV-8 LANA and MCPV large T proteins, all hinder the function of p53, a pivotal factor of the DNA damage response, and pRb, an oncosuppressor that prevents over-replication of the cellular DNA [10][11][12][13][14]. HHV-4 encodes for a plethora of early proteins with oncogenic potential; for instance, BARF1 and BCRF1 have antiapoptotic function and the viral DNAse enzyme can cause genomic instability, therefore induction of the lytic cycle can contribute to the development of malignant phenotypes [15]. Even during the lysogenic cycle, HHV-4 encodes for proteins and interfering RNAs that have oncogenic potential [16].Integration can disrupt the transcripti...

show abstract

“…Since then, many reports in the field have supported this viewpoint [ 7 – 13 ]. Our previous work showed that high-risk HPV types 16 and 18 were detected in esophageal tumors [ 14 ], and HPV18 was localized in human chromosome 8 in the EC109 cell line [ 15 ], these results indicates that HPV infection is a pathogenic factor for esophageal cancer.…”

Section: Introductionmentioning

confidence: 98%

Integration of human papillomavirus 16 in esophageal carcinoma samples

HaiE

et al. 2017

Infect Agents Cancer

Self Cite

View full text Add to dashboard Cite

BackgroundEsophageal carcinoma (EC) is one of the major cancers in China. In 1982, Syrjanen first hypothesized the relationship between human papillomavirus (HPV) infection and the development of esophageal cancer. Since then, many reports in the field have supported this viewpoint. This study investigated the etiological relationship between HPV infection and the occurrence of esophageal carcinoma at Tangshan City of the Hebei province in China.Methods189 samples of esophageal carcinoma patients were collected. DNA and RNA were isolated from samples, HPV DNA was detected by polymerase chain reaction (PCR) using My09/11 for HPV L1, and HPV16 was determined using type-specific primer sets for HPV16 E6. The HPV16 integration site was verified by amplification of papillomavirus oncogene transcripts, and HPV16 oncogene transcript products were ligated to the pMD-18 T vector and sequenced to confirm the physical location of HPV16 integration.Results168 HPV-positive samples were detected in 189 samples, and among them 76 specimens were HPV16 positive. Approximately 600 bp of the HPV16 oncogene transcript were detected in nine esophageal cancer samples. Sequence analysis revealed that HPV16 E7 integrated into human chromosome 2 in three samples, into human chromosome 5 in one sample, into human chromosome 6 in one sample, into human chromosome 8 in two samples, and into human chromosome 17 in two samples. The results verified that the integrated HPV16 E7 in five samples harbored one mutation of viral DNA compared with the HPV16 sequence provided in GenBank (K02718).ConclusionsThe high prevalence of HPV16 suggests that HPV16 may play an etiological role in the development of esophageal cancer. The integration of HPV16 into host cell chromosomes suggests that persistent HPV infection is key for esophageal epithelial cell malignant transformation and carcinogenesis.

show abstract

Integration of human papillomavirus 18 DNA in esophageal carcinoma 109 cells

Abstract: Integration of the HPV genome into the host cell chromosome suggests that persistent HPV infection is vital for malignant cell transformation and carcinogenesis.

Cited by 8 publications

References 23 publications

Integration sites of human papillomavirus 18 in esophageal cancer samples

Integration sites of human papillomavirus 18 in esophageal cancer samples

Proportion of Transcriptionally Active Dna Virus Integrants: A Meta-Analysis

Integration of human papillomavirus 16 in esophageal carcinoma samples

Contact Info

Product

Resources

About