Evidence map›Paper›PMID 26863632›Full record

ArticleOncotarget2016

Oncogenic potential of histone-variant H2A.Z.1 and its regulatory role in cell cycle and epithelial-mesenchymal transition in liver cancer.

Hee Doo Yang, Pum-Joon Kim, Jung Woo Eun, Qingyu Shen, Hyung Seok Kim, Woo Chan Shin, Young Min Ahn, Won Sang Park, Jung Young Lee, Suk Woo Nam

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

57 citing papers in PubMed, 83 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

10 authors at 2 institutions in 1 country.

Hee Doo YangLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Pum-Joon KimDepartment of Cardiology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Jung Woo EunLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Qingyu ShenLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Hyung Seok KimLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Woo Chan ShinLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Young Min AhnDepartment of Kidney System, College of Oriental Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.
Won Sang ParkLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Jung Young LeeLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Suk Woo NamLaboratory of Oncogenomics, Department of Pathology, College of Medicine, The Catholic University of Korea, Seoul 06591, Republic of Korea.
Catholic University of Korea · KRKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

H2A.Z is a highly conserved H2A variant, and two distinct H2A.Z isoforms, H2A.Z.1 and H2A.Z.2, have been identified as products of two non-allelic genes, H2AFZ and H2AFV. H2A.Z has been reported to be overexpressed in breast, prostate and bladder cancers, but most studies did not clearly distinguish between isoforms. One recent study reported a unique role for the H2A.Z isoform H2A.Z.2 as a driver of malignant melanoma. Here we first report that H2A.Z.1 plays a pivotal role in the liver tumorigenesis by selectively regulating key molecules in cell cycle and epithelial-mesenchymal transition (EMT). H2AFZ expression was significantly overexpressed in a large cohort of hepatocellular carcinoma (HCC) patients, and high expression of H2AFZ was significantly associated with their poor prognosis. H2A.Z.1 overexpression was demonstrated in a subset of human HCC and cell lines. H2A.Z.1 knockdown suppressed HCC cell growth by transcriptional deregulation of cell cycle proteins and caused apoptotic cell death of HCC cells. We also observed that H2A.Z.1 knockdown reduced the metastatic potential of HCC cells by selectively modulating epithelial-mesenchymal transition regulatory proteins such as E-cadherin and fibronectin. In addition, H2A.Z.1 knockdown reduced the in vivo tumor growth rate in a mouse xenograft model. In conclusion, our findings suggest the oncogenic potential of H2A.Z.1 in liver tumorigenesis and that it plays established role in accelerating cell cycle transition and EMT during hepatocarcinogenesis. This makes H2A.Z.1 a promising target in liver cancer therapy.

Indexed as

AnimalsCarcinoma, HepatocellularCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHep G2 CellsHeterograftsHistonesHumansLiver NeoplasmsMaleMiceMice, NudeTransfectionhistone H2A.F-ZHistonescell cycleepithelial-mesenchymal transitionH2A.Z.1liver cancer

Identifiers

PMID26863632
PMCPMC4905482
OpenAlexW2296375307

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.