Evidence map›Paper›PMID 27584795›Full record

ArticleCell death & disease2016

Overexpression of JARID1B promotes differentiation via SHIP1/AKT signaling in human hypopharyngeal squamous cell carcinoma.

Jisheng Zhang, Xiaofei An, Yafei Han, Rui Ma, Kun Yang, Lu Zhang, Jingwei Chi, Wei Li, David Llobet-Navas, Yan Xu and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

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  15. Article
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

11 authors at 4 institutions in 2 countries.

Jisheng ZhangKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Xiaofei AnDepartment of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, 155 Han Zhong Road, Nanjing 210029, China.
Yafei HanKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Rui MaDepartment of Nephrology, Affiliated Hospital of Qingdao University, Qingdao 266 003, China.
Kun YangKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Lu ZhangKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Jingwei ChiKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Wei LiKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
David Llobet-NavasInstitute of Genetic Medicine-Newcastle University, Newcastle upon Tyne NE1 3BZ, UK.
Yan XuDepartment of Nephrology, Affiliated Hospital of Qingdao University, Qingdao 266 003, China.
Yan JiangKey Laboratory, Department of Otolaryngology-Head and Neck Surgery, Affiliated Hospital of Qingdao University, Qingdao, Shandong 266003, China.
Affiliated Hospital of Qingdao University · CNQingdao University · CNJiangsu Province Hospital · CNNewcastle University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone H3 (H3K4) demethylase JARID1B is aberrantly upregulated in many types of tumor and has been proposed to function as oncogene. Here we show that JARID1B is elevated in moderate and high-differentiated human hypopharyngeal squamous cell carcinoma (HPSCC) compared with low-differentiated HPSCC. Overexpression of JARID1B in FaDu cells increased epithelial differentiation marker K10 expression and inhibited cell proliferation. JARID1B and K10 mRNA expression is high correlated in HPSCC patients. Mechanistically, we found JARID1B directly bound to PI3K/AKT signaling inhibitor SHIP1 gene promoter and decreased SHIP1 gene expression. Activation of downstream AKT resulted in increased β-catenin signaling, by which promoted target genes Fra-1 and Jun, together with other AP-1 transcription factors, leading to K10 expression. Forced expression of SHIP1 rescued JARID1B-induced phenotypes on FaDu cell differentiation and proliferation. Taken together, our findings provide first evidence that elevated expression of JARID1B has a critical role in promoting HPSCC differentiation and inhibiting proliferation, suggesting JARID1B may function as a tumor suppressor in squamous cell cancers and implying a novel important therapeutic strategy of HPSCC.

Indexed as

Cell DifferentiationSignal Transductionbeta CateninCarcinoma, Squamous CellCell Line, TumorDown-RegulationEnzyme ActivationGene Expression Regulation, NeoplasticGene Knockdown TechniquesHumansHypopharyngeal NeoplasmsJumonji Domain-Containing Histone DemethylasesKeratin-10Nuclear ProteinsPhenotypePhosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatasesbeta CateninINPP5D protein, humanJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanKeratin-10Nuclear ProteinsPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesProto-Oncogene Proteins c-aktRepressor Proteins

Identifiers

PMID27584795
PMCPMC5059865
OpenAlexW2512307284

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.