Evidence map›Paper›PMID 26170459›Full record

ArticleThe Journal of biological chemistry2015

Transcriptional activation of human CDCA8 gene regulated by transcription factor NF-Y in embryonic stem cells and cancer cells.

Can Dai, Cong-Xiu Miao, Xiao-Ming Xu, Lv-Jun Liu, Yi-Fan Gu, Di Zhou, Lian-Sheng Chen, Ge Lin, Guang-Xiu Lu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed, 94 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Can DaiFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078, the National Engineering and Research Center of Human Stem Cell, Changsha 410205, and the School of Basic Medical Science, Central South University, Changsha 410013, China.
Cong-Xiu MiaoFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078.
Xiao-Ming XuFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078.
Lv-Jun LiuFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078.
Yi-Fan GuFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078, the School of Basic Medical Science, Central South University, Changsha 410013, China.
Di ZhouFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078.
Lian-Sheng Chenthe National Engineering and Research Center of Human Stem Cell, Changsha 410205, and.
Ge LinFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078, the National Engineering and Research Center of Human Stem Cell, Changsha 410205, and linge_csu@yahoo.com.
Guang-Xiu LuFrom the Institute of Reproductive and Stem Cell Engineering, Central South University, Changsha 410078, the National Engineering and Research Center of Human Stem Cell, Changsha 410205, and lugxdirector@aliyun.com.
Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cell division cycle associated 8 (CDCA8) gene plays an important role in mitosis. Overexpression of CDCA8 was reported in some human cancers and is required for cancer growth and progression. We found CDCA8 expression was also high in human ES cells (hESCs) but dropped significantly upon hESC differentiation. However, the regulation of CDCA8 expression has not yet been studied. Here, we characterized the CDCA8 promoter and identified its cis-elements and transcription factors. Three transcription start sites were identified. Reporter gene assays revealed that the CDCA8 promoter was activated in hESCs and cancer cell lines. The promoter drove the reporter expression specifically to pluripotent cells during early mouse embryo development and to tumor tissues in tumor-bearing mice. These results indicate that CDCA8 is transcriptionally activated in hESCs and cancer cells. Mechanistically, two key activation elements, bound by transcription factor NF-Y and CREB1, respectively, were identified in the CDCA8 basic promoter by mutation analyses and electrophoretic motility shift assays. NF-Y binding is positively correlated with promoter activities in different cell types. Interestingly, the NF-YA subunit, binding to the promoter, is primarily a short isoform in hESCs and a long isoform in cancer cells, indicating a different activation mechanism of the CDCA8 transcription between hESCs and cancer cells. Finally, enhanced CDCA8 promoter activities by NF-Y overexpression and reduced CDCA8 transcription by NF-Y knockdown further verified that NF-Y is a positive regulator of CDCA8 transcription. Our study unearths the molecular mechanisms underlying the activation of CDCA8 expression in hESCs and cancer cells, which provides a better understanding of its biological functions.

Indexed as

Gene Expression Regulation, NeoplasticPromoter Regions, GeneticTranscriptional ActivationAnimalsCCAAT-Binding FactorCell Cycle ProteinsCell DifferentiationEmbryo, MammalianEmbryonic Stem CellsGene Knockdown TechniquesHeLa CellsHeterograftsHumansHuman Umbilical Vein Endothelial CellsMiceMice, TransgenicCCAAT-Binding FactorCDCA8 protein, humanCell Cycle ProteinsNFYA protein, humancancerCDCA8differentiationembryonic stem cellNF-Ypromotertranscription

Identifiers

PMID26170459
PMCPMC4566217
OpenAlexW1510199949

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.