Evidence map›Paper›PMID 38263342›Full record

ArticleJournal of cancer research and clinical oncology2024

Human papillomavirus E7 protein induces homologous recombination defects and PARPi sensitivity.

Siqi He, Ao Wang, Jing Wang, Zizhi Tang, Xiaojun Wang, Danqing Wang, Jie Chen, Cong Liu, Mingcai Zhao, Hui Chen and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cancer research and clinical oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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  5. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Siqi He *Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Ao Wang *Key Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Jing Wang *Department of Clinical Laboratory, Suining Central Hospital, Suining, 629000, People's Republic of China.
Zizhi TangKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Xiaojun WangKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Danqing WangKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Jie ChenKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Cong LiuKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China.
Mingcai ZhaoDepartment of Clinical Laboratory, Suining Central Hospital, Suining, 629000, People's Republic of China. 112068366@qq.com.
Hui ChenKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China. chenhui2022@scu.edu.cn.
Liang SongKey Laboratory of Birth Defects and Related Diseases of Women and Children (Ministry of Education), Department of Gynecology and Obstetrics, Meishan Women and Children's Hospital, West China Second University Hospital, Sichuan University, Chengdu, 610041, People's Republic of China. drsongliang@163.com.
Sichuan University · CNSuizhou Central Hospital · CN

Funding

Department of Science and Technology of Sichuan Province 2019JDTD0020Department of Science and Technology of Sichuan Province 2020YFH0019Department of Science and Technology of Sichuan Province 2022NSFSC1502Department of Science and Technology of Sichuan Province 2023NSFSC0738Sichuan University 2020SCUNL204Sichuan University 22H0851Sichuan University SCU2019C4198The National Natural Science Foundation of China 81821002
6 · The paper itself

Abstract

purposeCervical cancer is a common gynecological malignancy, pathologically associated with persistent infection of high-risk types of human papillomavirus (HPV). Previous studies revealed that HPV-positive cervical cancer displays genomic instability; however, the underlying mechanism is not fully understood.

methodsTo investigate if DNA damage responses are aggravated in precancerous lesions of HPV-positive cervical epithelium, cervical tissues were biopsied and cryosectioned, and subjected to immunofluorescent staining. Cloned HA-tagged E6 and E7 genes of HPV16 subtype were transfected into HEK293T or C33A cells, and indirect immunofluorescent staining was applied to reveal the competency of double strand break (DSB) repair. To test the synthetic lethality of E7-indued HRD and PARP inhibitor (PARPi), we expressed E7 in C33A cells in the presence or absence of olaparib, and evaluated cell viability by colony formation.

resultsIn precancerous lesions, endogenous DNA lesions were elevated along with the severity of CIN grade. Expressing high-risk viral factor (E7) in HPV-negative cervical cells did not impair checkpoint activation upon genotoxic insults, but affected the potential of DSB repair, leading to homologous recombination deficiency (HRD). Based on this HPV-induced genomic instability, the viability of E7-expressing cells was reduced upon exposure to PARPi in comparison with control cells.

conclusionIn aggregate, our findings demonstrate that HPV-E7 is a potential driver for genome instability and provides a new angle to understand its role in cancer development. The viral HRD could be employed to target HPV-positive cervical cancer via synthetic lethality.

Indexed as

Antineoplastic AgentsPapillomavirus InfectionsPrecancerous ConditionsUterine Cervical NeoplasmsFemaleGenomic InstabilityHEK293 CellsHuman Papillomavirus VirusesHumansPapillomaviridaePoly(ADP-ribose) Polymerase InhibitorsAntineoplastic AgentsPoly(ADP-ribose) Polymerase Inhibitorscervical cancerCheckpointDNA repairHPVPARP inhibitor

Identifiers

PMID38263342
PMCPMC10805821
OpenAlexW4391145752

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.