Evidence map›Paper›PMID 27314680›Full record

ArticleMolecular medicine reports2016

Silencing cyclin-dependent kinase inhibitor 3 inhibits the migration of breast cancer cell lines.

Miao Deng, Jianguang Wang, Yanbin Chen, Like Zhang, Gangqiang Xie, Qipeng Liu, Ting Zhang, Pengfei Yuan, Dechun Liu

RetractedOpen access · hybridAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 14% 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, 26 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Miao DengDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Jianguang WangDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Yanbin ChenDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Like ZhangDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Gangqiang XieDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Qipeng LiuDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Ting ZhangDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Pengfei YuanDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
Dechun LiuDepartment of Breast Surgery, The First Affiliated Hospital of Henan University of Science and Technology, Luoyang, Henan 471003, P.R. China.
First Affiliated Hospital of Henan University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin-dependent kinase inhibitor 3 (CDKN3) belongs to the dual-specificity protein phosphatase family, which is hypothesized to regulate cell cycle progression in tumor cells. However, whether CDKN3 is a potential therapeutic target for breast cancer remains to be elucidated. The present in vitro study aimed to investigate the potential roles of CDKN3 in breast cancer. Breast cancer cell lines were used to detect CDKN3 expression, and CDKN3 expression was silenced to investigate its role in cell apoptosis, cell cycle arrest and migration. The underlying mechanisms were screened by detecting proliferating cell nuclear antigen (PCNA), Ras homolog gene family, member A (RhoA), vimentin, B‑cell lymphoma 2 (Bcl‑2) and Bcl‑2‑associated X protein (Bax) expression. CDKN3 was highly expressed in MCF‑7 and BT474 cell lines. The silencing of CDKN3 in MCF‑7 and BT474 cell lines promoted cell apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. The expression levels of PCNA, RhoA, vimentin and Bcl‑2 were downregulated following CDKN3 silencing. Conversely, Bax expression was increased, as compared with the vehicle control. These results suggest that CDKN3 acts as an oncogene during breast cancer progression. The in vitro silencing of CDKN3 promoted apoptosis, induced G1 phase cell cycle arrest and inhibited cell migration. Possible mechanisms are associated with the regulation of PCNA, Bcl‑2, vimentin, RhoA and Bax expression. CDKN3 may therefore be considered a potential target for the treatment of breast cancer.

Indexed as

Gene SilencingApoptosisbcl-2-Associated X ProteinBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationCyclin-Dependent Kinase Inhibitor ProteinsDual-Specificity PhosphatasesFemaleGene Knockdown TechniquesHumansProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2rhoA GTP-Binding Proteinbcl-2-Associated X ProteinCDKN3 protein, humanCyclin-Dependent Kinase Inhibitor ProteinsDual-Specificity PhosphatasesProliferating Cell Nuclear AntigenProto-Oncogene Proteins c-bcl-2rhoA GTP-Binding ProteinRNA, Small Interfering

Identifiers

PMID27314680
PMCPMC4940103
OpenAlexW2442995819

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.