Evidence map›Paper›PMID 25333262›Full record

ArticleOncotarget2014

CDKL2 promotes epithelial-mesenchymal transition and breast cancer progression.

Linna Li, Chunping Liu, Robert J Amato, Jeffrey T Chang, Guangwei Du, Wenliang Li

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Prognostic Significance ofMedicina (Kaunas, Lithuania) · 2026
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  13. DecreasedFrontiers in molecular biosciences · 2021
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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

6 authors at 4 institutions in 2 countries.

Linna LiTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas. Department of Pharmacology and Toxicology, Beijing Institute of Radiation Medicine, Beijing, China.
Chunping LiuTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas.
Robert J AmatoDivision of Oncology, Department of Internal Medicine, and Memorial Hermann Cancer Center, University of Texas Health Science Center at Houston, Houston, Texas.
Jeffrey T ChangDepartment of Integrative Biology and Pharmacology, School of Medicine, University of Texas Health Science Center at Houston, Houston, Texas. School of Biomedical Informatics, University of Texas Health Science Center at Houston, Houston, Texas.
Guangwei DuDepartment of Integrative Biology and Pharmacology, School of Medicine, University of Texas Health Science Center at Houston, Houston, Texas.
Wenliang LiTexas Therapeutics Institute, Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, Texas. Division of Oncology, Department of Internal Medicine, and Memorial Hermann Cancer Center, University of Texas Health Science Center at Houston, Houston, Texas. Cancer Biology Program, Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, Texas.
The University of Texas Health Science Center at Houston · USBeijing Radiation Center · CNBrown Foundation · USMemorial Hermann · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epithelial-mesenchymal transition (EMT) confers mesenchymal properties on epithelial cells and has been closely associated with the acquisition of aggressive traits by epithelial cancer cells. To identify novel regulators of EMT, we carried out cDNA screens that covered 500 human kinases. Subsequent characterization of candidate kinases led us to uncover cyclin-dependent kinase-like 2 (CDKL2) as a novel potent promoter for EMT and breast cancer progression. CDKL2-expressing human mammary gland epithelial cells displayed enhanced mesenchymal traits and stem cell-like phenotypes, which was acquired through activating a ZEB1/E-cadherin/β-catenin positive feedback loop and regulating CD44 mRNA alternative splicing to promote conversion of CD24(high) cells to CD44(high) cells. Furthermore, CDKL2 enhanced primary tumor formation and metastasis in a breast cancer xenograft model. Notably, CDKL2 is expressed significantly higher in mesenchymal human breast cancer cell lines than in epithelial lines, and its over-expression/amplification in human breast cancers is associated with shorter disease-free survival. Taken together, our study uncovered a major role for CDKL2 in promoting EMT and breast cancer progression.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsApoptosisbeta CateninBlotting, WesternBreast NeoplasmsCadherinsCalcium-Calmodulin-Dependent Protein KinasesCell ProliferationCyclin-Dependent KinasesDisease ProgressionFemaleFlow CytometryHomeodomain ProteinsHumansImmunoenzyme Techniquesbeta CateninCadherinsCalcium-Calmodulin-Dependent Protein KinasesCDKL2 protein, humanCyclin-Dependent KinasesHomeodomain ProteinsTranscription FactorsZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1

Identifiers

PMID25333262
PMCPMC4279414
OpenAlexW1542528628

What OpenQuestion holds

Textmetadata
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.