Evidence map›Paper›PMID 25239643›Full record

ArticleCarcinogenesis2015

The role of miR-200a in mammalian epithelial cell transformation.

Lindsey E Becker, Apana Agha L Takwi, Zhongxin Lu, Yong Li

Open access · greenAbstract read
In one paragraph

Article in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

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  13. Tumor suppressive microRNA-200a inhibits renal cell carcinoma development by directly targeting TGFB2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
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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

4 authors at 3 institutions in 2 countries.

Lindsey E BeckerDepartment of Biochemistry and Molecular Biology, School of Medicine, University of Louisville, 319 Abraham Flexner Way, Louisville, KY 40202, USA.
Apana Agha L TakwiSt Jude Children's Research Hospital, 262 Danny Thomas Place, Memphis, TN 38105, USA and.
Zhongxin LuDepartment of Medical Laboratory and Central Laboratory, The Central Hospital of Wuhan, Wuhan, Hubei 430014, China.
Yong LiDepartment of Biochemistry and Molecular Biology, School of Medicine, University of Louisville, 319 Abraham Flexner Way, Louisville, KY 40202, USA, Department of Medical Laboratory and Central Laboratory, The Central Hospital of Wuhan, Wuhan, Hubei 430014, China yong.li@louisville.edu.
University of Louisville · USCentral Hospital of Wuhan · CNSt. Jude Children's Research Hospital · US

Funding

UOFL ENVIRONMENTAL HEALTH SCIENCES TRAINING PROGRAMT32ES011564 · NIEHS · UNIVERSITY OF LOUISVILLE · PI David W Hein, John Pierce Wise · 2004 to 2026
$7.1M
Convergence of MicroRNAs and p53 Signaling in Multiple Myeloma: Environmental CoR01CA138688 · NCI · UNIVERSITY OF LOUISVILLE · PI LI, YONG · 2009 to 2017
$2.9M
NCI NIH HHS R01 CA138688NIEHS NIH HHS T32-ES011564
6 · The paper itself

Abstract

Cancer is a multistep disease that begins with malignant cell transformation and frequently culminates in metastasis. MicroRNAs (miRNAs) are small regulatory 21-25 nt RNA molecules and are frequently deregulated in cancer. miR-200a is a member of the miR-200 family, which are known inhibitors of the epithelial-to-mesenchymal transition. As such, the tumor-suppressive role of miR-200a in oncogenesis has been well documented; however, recent studies have found a proliferative role for this miRNA as well as a prometastatic role in the later steps of cancer progression. Little is known about the role of this miRNA in the early stages of cancer, namely, malignant cell transformation. Here, we show that miR-200a alone transforms an immortalized rat epithelial cell line, and miR-200a cooperates with Ras to enhance malignant transformation of an immortalized human epithelial cell line. Furthermore, miR-200a induces cell transformation and tumorigenesis in immunocompromised mice by cooperating with a Ras mutant that activates only the RalGEF effector pathway, but not Ras mutants activating PI3K or Raf effector pathways. This transformative ability is in accordance with miR-200a targeting Fog2 and p53 to activate Akt and directly repress p53 protein levels, respectively. These results demonstrate an oncogenic role for miR-200a and provide a specific cellular context where miR-200a acts as an oncomiR rather than a tumor suppressor by cooperating with an oncogene in malignant cell transformation.

Indexed as

AnimalsApoptosisBlotting, WesternBreastBreast NeoplasmsCell CycleCell MovementCell ProliferationCells, CulturedCell Transformation, NeoplasticEpithelial CellsFemaleHumansKidneyMaleMiceMicroRNAsMIRN200 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktral Guanine Nucleotide Exchange Factor

Identifiers

PMID25239643
PMCPMC4291045
OpenAlexW2334131957

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.