Evidence map›Paper›PMID 29925860›Full record

ArticleOncogene2018

MacroH2A1.2 inhibits prostate cancer-induced osteoclastogenesis through cooperation with HP1α and H1.2.

Jin-Man Kim, Yonghwan Shin, Sunyoung Lee, Mi Yeong Kim, Vasu Punj, Hong-In Shin, Kyunghwan Kim, Jung-Min Koh, Daewon Jeong, Woojin An

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.4field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 29 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 5 institutions in 2 countries.

Jin-Man KimDepartment of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Yonghwan ShinDepartment of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Sunyoung LeeDepartment of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Mi Yeong KimDepartment of Microbiology, College of Medicine, Yeungnam University, Daegu, 705-717, Republic of Korea.
Vasu PunjDepartment of Medicine, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Hong-In ShinDepartment of Oral Pathology, School of Dentistry, Kyungpook National University, Daegu, 700-412, Republic of Korea.
Kyunghwan KimDepartment of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Jung-Min KohDivision of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, Seoul, 138-736, Republic of Korea.
Daewon JeongDepartment of Microbiology, College of Medicine, Yeungnam University, Daegu, 705-717, Republic of Korea.
Woojin AnDepartment of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA. woojinan@usc.edu.
University of Southern California · USYeungnam University · KRAsan Medical Center · KRChungbuk National University · KRKyungpook National University · KR

Funding

Role of histone kinase VprBP in gene silencing: mechanisms, targets, and regulationR01CA201561 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI AN, WOOJIN · 2016 to 2020
$1.9M
NCI NIH HHS R01 CA201561
6 · The paper itself

Abstract

Osteoclasts are multinuclear bone-resorbing cells that differentiate from hematopoietic precursor cells. Prostate cancer cells frequently spread to bone and secrete soluble signaling factors to accelerate osteoclast differentiation and bone resorption. However, processes and mechanisms that govern the expression of osteoclastogenic soluble factors secreted by prostate cancer cells are largely unknown. MacroH2A (mH2A) is a histone variant that replaces canonical H2A at designated genomic loci and establishes functionally distinct chromatin regions. Here, we report that mH2A1.2, one of the mH2A isoforms, attenuates prostate cancer-induced osteoclastogenesis by maintaining the inactive state of genes encoding soluble factors in prostate cancer cells. Our functional analyses of soluble factors identify lymphotoxin beta (LTβ) as a major stimulator of osteoclastogenesis and an essential mH2A1.2 target for its anti-osteoclastogenic activity. Mechanistically, mH2A1.2 directly interacts with HP1α and H1.2 and requires them to inactivate LTβ gene in prostate cancer cells. Consistently, HP1α and H1.2 have an intrinsic ability to inhibit osteoclast differentiation in a mH2A1.2-dependent manner. Together, our data uncover a new and specific role for mH2A1.2 in modulating osteoclastogenic potential of prostate cancer cells and demonstrate how this signaling pathway can be exploited to treat osteolytic bone metastases at the molecular level.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBone NeoplasmsCell Line, TumorChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistonesHumansMaleMiceNeoplasm MetastasisNeoplasm ProteinsOsteoclastsOsteolysisProstatic NeoplasmsCBX5 protein, humanChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistonesmacroH2A histoneNeoplasm Proteins

Identifiers

PMID29925860
PMCPMC6309402
OpenAlexW2808981308

What OpenQuestion holds

Textmetadata
LicenceTDM
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.