Evidence map›Paper›PMID 29789527›Full record

ArticleCell death & disease2018

Regulator of chromatin condensation 1 abrogates the G1 cell cycle checkpoint via Cdk1 in human papillomavirus E7-expressing epithelium and cervical cancer cells.

Lijun Qiao, Jingyi Zheng, Yonghao Tian, Qishu Zhang, Xiao Wang, Jason J Chen, Weifang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 42 citations in OpenAlex.

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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

7 authors at 2 institutions in 1 country.

Lijun QiaoCancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Jingyi ZhengDepartment of Microbiology and Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Yonghao TianDepartment of Orthopedic Surgery, Qilu Hospital Affiliated Shandong University, Jinan, Shandong, China.
Qishu ZhangCancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Xiao WangInstitute of Pathobiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Jason J ChenCancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Weifang ZhangDepartment of Microbiology and Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China. zhangweifang@sdu.edu.cn.
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulator of chromatin condensation 1 (RCC1) is a major guanine-nucleotide exchange factor for Ran GTPase and plays key roles in nucleo-cytoplasmic transport, mitosis, and nuclear envelope assembly. RCC1 is known to be a critical cell cycle regulator whose loss causes G1 phase arrest, but the molecular basis for this regulation is poorly understood. Furthermore, little is known about the relationship between RCC1 and carcinomas. Human papillomavirus (HPV) infection is highly associated with the development of cervical cancer. The expression and function of RCC1 in HPV-related cervical cancer and cell cycle regulation have not yet been explored. In this study, we first observed that RCC1 immunostaining was mildly increased in cervical cancer tissues and significantly upregulated in HPV E7-expressing cells; this localization was primarily nuclear. We showed that the transcription factor c-Jun transcriptionally upregulates RCC1 via a direct interaction with the RCC1 promoter. Moreover, siRNA-mediated knockdown of RCC1 inhibited G1/S cell cycle progression and DNA synthesis, while overexpression of RCC1 abrogated the G1 checkpoint. RCC1 knockdown downregulated the protein levels of the transcription factor E2F1, especially nuclear E2F1, by promoting its degradation in HPV E7-expressing cells. Overexpression of E2F1 rescued RCC1 knockdown-mediated inhibition of G1/S progression. Additionally, we showed that cyclin-dependent kinase 1 (Cdk1), a known target of E2F1, is involved in G1 checkpoint regulation, as Cdk1 knockdown hindered G1/S progression, while Cdk1 overexpression rescued RCC1 knockdown-mediated effect on G1 cell cycle progression. Furthermore, RCC1 knockdown reduced HPV E7 protein levels, which may in turn downregulate E2F1. Our study explores the function of RCC1 in G1/S cell cycle progression and suggests that RCC1 may be involved in HPV E7-mediated genomic instability.

Indexed as

G1 Phase Cell Cycle Checkpoints3T3 CellsAnimalsCDC2 Protein KinaseCell Cycle ProteinsCell Line, TumorDNA ReplicationE2F1 Transcription FactorFemaleGene Expression Regulation, NeoplasticGuanine Nucleotide Exchange FactorsHumansMiceNuclear ProteinsPapillomavirus E7 ProteinsProteolysisCDC2 Protein KinaseCDK1 protein, humanCell Cycle ProteinsE2F1 Transcription FactorGuanine Nucleotide Exchange FactorsNuclear ProteinsPapillomavirus E7 ProteinsRCC1 protein, human

Identifiers

PMID29789527
PMCPMC5964113
OpenAlexW2804943893

What OpenQuestion holds

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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.