Evidence map›Paper›PMID 32848135›Full record

ArticleCell death & disease2020

ASF1B promotes cervical cancer progression through stabilization of CDK9.

Xinjian Liu, Jingwei Song, Yenan Zhang, Huiquan Wang, Hongzhi Sun, Xiaomin Feng, Min Hou, Guo Chen, Qi Tang, Minjun Ji

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 65 citations in OpenAlex.

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  16. The interaction betweenAnnals of medicine · 2023
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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

10 authors at 4 institutions in 1 country.

Xinjian Liu *Department of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Jingwei Song *Department of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Yenan ZhangDepartment of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Huiquan WangDepartment of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Hongzhi SunDepartment of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Xiaomin FengThe Affiliated Obstetrics and Gynecology Hospital of Nanjing Medical University, 210004, Nanjing, China.
Min HouDepartment of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China.
Guo ChenDepartment of Medical Biochemistry and Molecular Biology, School of Medicine, Jinan University, 510632, Guangzhou, China.
Qi TangKey Laboratory of Antibody Technique of National Health Commission of China, Nanjing Medical University, 211166, Nanjing, China.
Minjun JiDepartment of Pathogen Biology, Nanjing Medical University, 211166, Nanjing, China. jiminjun@njmu.edu.cn.ORCID http://orcid.org/0000-0003-0293-0255
Nanjing Medical University · CNNational Health and Family Planning Commission · CNJinan University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Recent studies have shown that anti-silencing function 1B (ASF1B) might be used as a new proliferation marker for cancer diagnosis and prognosis. However, the expression and function of ASF1B in cervical cancer remain unclear. Here, we induced ASF1B knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established two murine models using stable ASF1B-shRNA HeLa cells or normal HeLa cells following AAV-shRNA-ASF1B administration to evaluate how suppression of ASF1B affects tumor growth. We showed that ASF1B functions as an oncogene in cervical cancer cells. Silence of ASF1B suppressed cervical cancer cell growth in vitro and in vivo, while, ASF1B overexpression accelerated cancer cell proliferation. Furthermore, ASF1B deficiency induced cell cycle arrest and apoptosis. Mechanistically, we found that ASF1B formed stable complexes with cyclin-dependent kinase 9 (CDK9), and positively regulated CDK9 stabilization. Taken together, tumorigenic ASF1B could be targeted to suppress cervical cancer tumor growth by inducing apoptotic cell death.

Indexed as

AnimalsApoptosisCell CycleCell Cycle ProteinsCell Line, TumorCell ProliferationChinaCyclin-Dependent Kinase 9Disease Models, AnimalDisease ProgressionFemaleHeLa CellsHumansMiceMice, NudeOncogenesASF1B protein, humanCDK9 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase 9Proto-Oncogene Proteins c-aktRNA, Small Interfering

Identifiers

PMID32848135
PMCPMC7449975
OpenAlexW3080531908

What OpenQuestion holds

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LicenceCC BY
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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.