Evidence map›Paper›PMID 25909221›Full record

ArticleOncotarget2015

miR-497 and miR-34a retard lung cancer growth by co-inhibiting cyclin E1 (CCNE1).

Zhiyuan Han, Yanbin Zhang, Qiaoyuan Yang, Binbin Liu, Jianjun Wu, Yajie Zhang, Chengfeng Yang, Yiguo Jiang

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
2.9field-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

55 citing papers in PubMed, 91 citations in OpenAlex.

  1. Melatonin in lung cancer: integrating molecular mechanisms, tumor microenvironment regulation, apoptotic signaling, and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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  17. Frontiers in veterinary science · 2022
    Article
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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

8 authors at 3 institutions in 2 countries.

Zhiyuan HanState Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China.
Yanbin ZhangDepartment of Pulmonary Tuberculosis, Guangzhou Chest Hospital, Guangzhou, P.R. China.
Qiaoyuan YangState Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China.
Binbin LiuState Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China.
Jianjun WuState Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China.
Yajie ZhangDepartment of Pathology, Guangzhou Medical University, Guangzhou, P.R. China.
Chengfeng YangDepartment of Physiology and Center for Integrative Toxicology, Michigan State University, East Lansing, MI, USA.
Yiguo JiangState Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, Guangzhou Medical University, Guangzhou, P.R. China.
Guangzhou Medical University · CNState Key Laboratory of Respiratory Disease · CNMichigan State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cyclin E1, encoded by the CCNE1 gene, promotes G1/S transition, chromosome instability, and oncogenesis. Here, we show that miR-497 and miR-34a target the 3'-UTR of CCNE1. miR-497 and miR-34a are downregulated in cancer cells and their ectopic expression inhibited cell proliferation and colony formation in vitro, and inhibited tumor growth in a xenograft model. The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation, colony formation, and tumor growth, and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone. The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels. When cells stably expressing CCNE1 were transfected with the Hi-miR-497/34a plasmid, there was no effect on colony formation, compared with that of cells transfected with either Hi-miR497 or Hi-miR34a. These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a, which synergistically retard the growth of human lung cancer cells.

Indexed as

AnimalsCell Line, TumorCell ProliferationCyclin EDown-RegulationHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, NudeMicroRNAsOncogene ProteinsReal-Time Polymerase Chain ReactionCCNE1 protein, humanCyclin EMicroRNAsMIRN34 microRNA, humanMIRN497 microRNA, humanOncogene ProteinsCCNE1lung cancermiR-34amiR-497

Identifiers

PMID25909221
PMCPMC4537005
OpenAlexW1876719820

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.