Evidence map›Paper›PMID 35875100›Full record

ArticleFrontiers in oncology2022

HPV16 E6-Activated OCT4 Promotes Cervical Cancer Progression by Suppressing p53 Expression

Shujuan Shu, Zhi Li, Liu Liu, Xia Ying, Yina Zhang, Ting Wang, Xiaoye Zhou, Peiyue Jiang, Weiguo Lv

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Genome composition-based deep learning predicts oncogenic potential of HPVs.Frontiers in cellular and infection microbiology · 2024
    Article
  15. Article
  16. Pioneer factors in viral infection.Frontiers in immunology · 2023
    Review
  17. RNA NCell & bioscience · 2022
    Article
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

9 authors at 1 institution in 1 country.

Shujuan ShuDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Zhi LiDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Liu LiuDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Xia YingDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Yina ZhangDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Ting WangDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Xiaoye ZhouDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Peiyue JiangDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Weiguo LvDepartment of Obstetrics and Gynecology, Women's Hospital, Medicine School of Zhejiang University, Hangzhou, China.
Women's Hospital, School of Medicine, Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papillomaviruses (HPV), mainly HPV16 and HPV18, of high-risk classification are involved in cervical cancer carcinogenesis and progression. Octamer-binding transcription factor 4 (OCT4) is a key transcription factor that is increased in various cancer types. Cervical cancer patients with higher levels of OCT4 had worse survival rates. However, the definite mechanisms underlying its function in the development of cervical cancer still remain to be explicated. Here, our study demonstrated that OCT4 expression was slightly increased in cervical cancer tissues than in precancerous ones. However, OCT4 was significantly upregulated in HPV16-positive tissues, in contrast to the expression profiling for p53. Moreover, knockdown of HPV16 E6 in SiHa cells suppressed the expression of OCT4 with impaired activities of cell proliferation, migration, and invasion, while it recovered the expression of p53. Overexpression of OCT4 and p53 exerted opposite roles on cell proliferation, migration, invasion, and colony formation of cervical cancer cells. More importantly, the enforced expression of OCT4 augmented p53-inhibited cell migration, invasion, and colony formation in human cervical cancer by promoting EMT. Finally, we identified that OCT4 could bind to the

Indexed as

cervical cancerHPV16 E6malignant progressionNCOR1OCT4p53

Identifiers

PMID35875100
PMCPMC9302044
OpenAlexW4284893839

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.