Evidence map›Paper›PMID 27451945›Full record

ArticleScientific reports2016

ClC-3 Chloride Channel Proteins Regulate the Cell Cycle by Up-regulating cyclin D1-CDK4/6 through Suppressing p21/p27 Expression in Nasopharyngeal Carcinoma Cells.

Dong Ye, Hai Luo, Zhouyi Lai, Lili Zou, Linyan Zhu, Jianwen Mao, Tim Jacob, Wencai Ye, Liwei Wang, Lixin Chen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 37 citations in OpenAlex.

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  11. Ion Channel Dysregulation in Head and Neck Cancers: Perspectives for Clinical Application.Reviews of physiology, biochemistry and pharmacology · 2021
    Review
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  20. Curcumin suppresses gastric cancer biological activity by regulation of miRNA-21: an in vitro study.International journal of clinical and experimental pathology · 2018
    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

10 authors at 3 institutions in 2 countries.

Dong YeDepartment of Physiology, Guangdong Pharmaceutical University, Guangzhou, China.
Hai LuoDepartment of Physiology, Medical College, Jinan University, Guangzhou, China.
Zhouyi LaiDepartment of Physiology, Medical College, Jinan University, Guangzhou, China.
Lili ZouDepartment of Physiology, Medical College, Jinan University, Guangzhou, China.
Linyan ZhuDepartment of Pharmacology, Medical College, Jinan University, Guangzhou, China.
Jianwen MaoDepartment of Physiology, Guangdong Pharmaceutical University, Guangzhou, China.
Tim JacobCardiff School of Biosciences, Cardiff University, Cardiff, UK.
Wencai YeCollege of Pharmacy, Jinan University, Guangzhou, China.
Liwei WangDepartment of Physiology, Medical College, Jinan University, Guangzhou, China.
Lixin ChenDepartment of Pharmacology, Medical College, Jinan University, Guangzhou, China.
Jinan University · CNGuangdong Pharmaceutical University · CNCardiff University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It was shown in this study that knockdown of ClC-3 expression by ClC-3 siRNA prevented the activation of hypotonicity-induced chloride currents, and arrested cells at the G0/G1 phase in nasopharyngeal carcinoma CNE-2Z cells. Reconstitution of ClC-3 expression with ClC-3 expression plasmids could rescue the cells from the cell cycle arrest caused by ClC-3 siRNA treatments. Transfection of cells with ClC-3 siRNA decreased the expression of cyclin D1, cyclin dependent kinase 4 and 6, and increased the expression of cyclin dependent kinase inhibitors (CDKIs), p21 and p27. Pretreatments of cells with p21 and p27 siRNAs depleted the inhibitory effects of ClC-3 siRNA on the expression of CDK4 and CDK6, but not on that of cyclin D1, indicating the requirement of p21 and p27 for the inhibitory effects of ClC-3 siRNA on CDK4 and CDK6 expression. ClC-3 siRNA inhibited cells to progress from the G1 phase to the S phase, but pretreatments of cells with p21 and p27 siRNAs abolished the inhibitory effects of ClC-3 siRNA on the cell cycle progress. Our data suggest that ClC-3 may regulate cell cycle transition between G0/G1 and S phases by up-regulation of the expression of CDK4 and CDK6 through suppression of p21 and p27 expression.

Indexed as

CarcinomaCell CycleCell Line, TumorChloride ChannelsCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27Gene Expression Regulation, NeoplasticHumansNasopharyngeal CarcinomaNasopharyngeal NeoplasmsRNA, Small InterferingS PhaseTranscriptional ActivationCCND1 protein, humanCDK4 protein, humanCDK6 protein, humanChloride ChannelsClC-3 channelCyclin D1Cyclin-Dependent Kinase 4Cyclin-Dependent Kinase 6Cyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent Kinase Inhibitor p27RNA, Small Interfering

Identifiers

PMID27451945
PMCPMC4959003
OpenAlexW2497477623

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.