Evidence map›Paper›PMID 34387848›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2021

MiR-495-3p and miR-143-3p co-target CDK1 to inhibit the development of cervical cancer.

J Tang, H Pan, W Wang, C Qi, C Gu, A Shang, J Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  5. lncRNA FENDRR Predicts Adverse Prognosis and Regulates the Development of Esophageal Squamous Cell Carcinoma Through Negatively Modulating miR-495-3p.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025
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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 4 institutions in 1 country.

J Tang *Department of Gynecology and Obstetrics, Huzhou Central Hospital, Affiliated Central Hospital of Huzhou Normal University, Huzhou, 313003, People's Republic of China.
H Pan *Department of Laboratory Medicine, Shanghai Simple Gene Medical Laboratory, Shanghai, 200025, People's Republic of China.
W Wang *Department of Pathology, The Sixth People's Hospital of Yancheng City, Yancheng, 224005, People's Republic of China.
C QiDepartment of Pathology, The Sixth People's Hospital of Yancheng City, Yancheng, 224005, People's Republic of China.
C GuDepartment of Laboratory Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, People's Republic of China.
A ShangDepartment of Pathology, The Sixth People's Hospital of Yancheng City, Yancheng, 224005, People's Republic of China. shanganquan@sina.com.ORCID http://orcid.org/0000-0003-2820-1982
J ZhuDepartment of Laboratory Medicine, Huzhou Central Hospital, Affiliated Central Hospital of Huzhou Normal University, Huzhou, 313003, Zhejiang Province, People's Republic of China. hz_zhujichao@yeah.net.
Huzhou Central Hospital · CNNantong University · CNTongji University · CNShanghai International Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThe GEO database and KEGG database-based analyses identified the differential expression of cyclin-dependent kinase 1 (CDK1) in cervical cancer and its involvement in the cell cycle pathway. In the present study, we aim to clarify the role of CDK1 in cervical cancer and the function of upstream microRNA (miR)-143-3p/miR-495-3p.

methodsThe expression of miR-143-3p, miR-495-3p, and CDK1 in cervical cancer tissues and cells was determined using RT-qPCR. Cell bioactivities were examined by CCK-8 and flow cytometry. The binding affinity between CDK1 and miR-143-3p/miR-495-3p was investigated using dual luciferase gene reporter assay. A xenograft mouse model of cervical cancer was then established to explore their effect on the tumorigenicity of cervical cancer cells in vivo.

resultsCDK1 was found to be the common target gene of miR-143-3p and miR-495-3p. CDK1 overexpression occurred in cervical cancer tissues and cells, while expression of miR-495-3p and miR-143-3p was down-regulated. The viability was inhibited while the apoptosis was promoted in cervical cancer cells in response to miR-143-3p or miR-495-3p overexpression, or CDK1 silencing. Further, miR-143-3p or miR-495-3p overexpression was also substantiated to inhibit the tumorigenicity of cervical cancer cells in vivo, while CDK1 overexpression counteracted their effect.

conclusionTaken together, miR-143-3p and miR-495-3p co-target CDK1, thereby inhibiting the occurrence and development of cervical cancer.

Indexed as

AnimalsApoptosisCDC2 Protein KinaseCell CycleCell MovementCell ProliferationCervix UteriDatabases, GeneticDown-RegulationFemaleGene SilencingGenes, ReporterHeLa CellsHeterograftsHumansLuciferasesCDC2 Protein KinaseCDK1 protein, humanLuciferasesMicroRNAsMIRN143 microRNA, humanMIRN495 microRNA, humanApoptosisCDK1Cervical cancermiR-143-3pmiR-495-3pProliferation

Identifiers

PMID34387848
OpenAlexW3187499996

What OpenQuestion holds

Textmetadata
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.