Evidence map›Paper›PMID 33544437›Full record

ArticleCancer science2021

MOF upregulates the estrogen receptor α signaling pathway by its acetylase activity in hepatocellular carcinoma.

Shan Wei, Wei Liu, Ning Sun, Yi Wu, Huijuan Song, Chunyu Wang, Shengli Wang, Renlong Zou, Lin Lin, Kai Zeng and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 22 citations in OpenAlex.

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  8. A multidimensional pan-cancer analysis of DCAF13 and its protumorigenic effect in lung adenocarcinoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
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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

15 authors at 3 institutions in 1 country.

Shan WeiDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Wei LiuDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Ning SunDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Yi WuDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Huijuan SongDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Chunyu WangDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Shengli WangDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Renlong ZouDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Lin LinDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Kai ZengDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Baosheng ZhouDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Manlin WangDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Ruina LuanDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Fan YangDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.
Yue ZhaoDepartment of Cell Biology, Key laboratory of Cell Biology, Ministry of Public Health, China Medical University, Shenyang, China.ORCID https://orcid.org/0000-0001-8983-0024
China Medical University · CNLiaoning Cancer Hospital & Institute · CNShenyang Medical College · CN

Funding

973 Program Grant from the Ministry of Science and Technology of China 2013CB945201Foundation for Special Professor of Liaoning Province for Yue ZhaoMinistry of Education fund innovation team IRT 13101National Natural Science Foundation of China 31701102National Natural Science Foundation of China 31871286National Natural Science Foundation of China 81702800National Natural Science Foundation of China 81872015
6 · The paper itself

Abstract

The histone acetyltransferase MOF (KAT8) is mainly involved in the acetylation of histone H4 at lysine 16 (H4K16) and some non-histone proteins. The MOF expression level is significantly reduced in many cancers, however the biological function of MOF and its underlying mechanism are still elusive in hepatocellular carcinoma (HCC). Estrogen receptor α (ERα) has been considered as a tumor suppressor in HCC. Here, we demonstrated that MOF expression is significantly reduced in HCC samples, and is positively correlated with that of ERα. MOF interacts with ERα, and participates in acetylation of ERα at K266, K268, K299, thereby inhibiting ERα ubiquitination to maintain the stability of ERα. In addition, MOF participates in the upregulation of ERα-mediated transactivation. Depletion of MOF significantly promotes cell growth, migration, and invasion in HCC cell lines. Taken together, our results provide new insights to understand the mechanism underlying the modulation function of MOF on ERα action in HCC, suggesting that MOF might be a potential therapeutic target for HCC.

Indexed as

AcetylationAcetylesteraseAnimalsAntibodiesCarcinoma, HepatocellularCell MovementCell ProliferationDatabases, GeneticDown-RegulationEstrogen Receptor alphaFemaleHeterograftsHistone AcetyltransferasesHistonesHumansKaplan-Meier EstimateAcetylesteraseAntibodiesESR1 protein, humanEstrogen Receptor alphaHistone AcetyltransferasesHistonesKAT8 protein, humanLysineacetylationestrogen receptor αhepatocellular carcinomaMOFtumor suppression

Identifiers

PMID33544437
PMCPMC8088912
OpenAlexW3128017792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.