Evidence map›Paper›PMID 35639349›Full record

ArticleCancer science2022

H1.0 induces paclitaxel-resistance genes expression in ovarian cancer cells by recruiting GCN5 and androgen receptor.

Abhidha Kohli, Shang-Lang Huang, Ting-Chang Chang, Chuck C-K Chao, Nian-Kang Sun

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

Article in Cancer science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

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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

10 citing papers in PubMed, 13 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

5 authors at 3 institutions in 1 country.

Abhidha KohliDepartment of Biochemistry and Molecular Biology, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan, Republic of China.
Shang-Lang HuangDivision of Biomedical Sciences, Chang Gung University of Science and Technology, Taoyuan, Taiwan, Republic of China.
Ting-Chang ChangDepartment of Obstetrics and Gynaecology, Chang Gung Memorial Hospital Linkou Medical Centre, Taoyuan, Taiwan, Republic of China.
Chuck C-K ChaoDepartment of Biochemistry and Molecular Biology, Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan, Republic of China.
Nian-Kang SunDivision of Biomedical Sciences, Chang Gung University of Science and Technology, Taoyuan, Taiwan, Republic of China.ORCID https://orcid.org/0000-0003-0924-3749
Chang Gung University · TWChang Gung University of Science and Technology · TWChang Gung Memorial Hospital · TW

Funding

Chang Gung Memorial Hospital BMRP071Chang Gung Memorial Hospital CMRPD3E0092Chang Gung Memorial Hospital CMRPF1K0101Chang Gung University of Science and Technology ZRRPF3L0091Ministry of Science and Technology of Taiwan MOST106-2320-B-255-004
6 · The paper itself

Abstract

More than 90% of ovarian cancer deaths are due to relapse following development of chemoresistance. Our main objective is to better understand the molecular mechanism underlying paclitaxel resistance (taxol resistance, Txr) in ovarian cancer. Here, we observed that the linker histone H1.0 is upregulated in paclitaxel-resistant ovarian cancer cells. Knockdown of H1.0 significantly downregulates the androgen receptor (AR) and sensitizes paclitaxel-resistant SKOV3/Txr and 2774/Txr cell lines to paclitaxel. Conversely, ectopic expression of H1.0 upregulates AR and increases Txr in parental SKOV3 and MDAH2774 cells. Notably, H1.0 upregulation is associated with disease recurrence and poor survival in a subset of ovarian cancer subjects. Inhibition of PI3K significantly reduces H1.0 mRNA and protein levels in paclitaxel-resistant cells, suggesting the involvement of the PI3K/AKT signaling pathway. Knockdown of H1.0 and AR also downregulates the Txr genes ABCB1 and ABCG2 in paclitaxel-resistant cells. Our data show that H1.0 induces GCN5 expression and histone acetylation, thereby enhancing Txr gene transactivation. These findings suggest that Txr in ovarian cancer involves the PI3K/AKT pathway and leads to upregulation of histone H1.0, recruitment of GCN5 and AR, followed by upregulation of a subgroup of Txr genes that include ABCB1 and ABCG2. This study is the first report describing the relationship between histone H1.0 and GCN5 that cooperate to induce AR-dependent Txr in ovarian cancer cells.

Indexed as

Drug Resistance, NeoplasmOvarian Neoplasmsp300-CBP Transcription FactorsPaclitaxelReceptors, AndrogenCell Line, TumorFemaleGene Expression Regulation, NeoplasticHistonesHumansNeoplasm Recurrence, Localp300-CBP-Associated FactorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAR protein, humanHistonesp300-CBP-Associated Factorp300-CBP Transcription FactorsPaclitaxelPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Androgenandrogen receptorGCN5H1.0ovarian cancerpaclitaxel resistance

Identifiers

PMID35639349
PMCPMC9357662
OpenAlexW4281765315

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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.