Evidence map›Paper›PMID 26389696›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

Liganded ERα Stimulates the E3 Ubiquitin Ligase Activity of UBE3C to Facilitate Cell Proliferation.

Maiko Okada, Fumiaki Ohtake, Hiroyuki Nishikawa, Wenwen Wu, Yasushi Saeki, Keiji Takana, Tomohiko Ohta

Abstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. The crosstalk between ubiquitination and endocrine therapy.Journal of molecular medicine (Berlin, Germany) · 2023
    Review
  3. Article
  4. Article
  5. Review
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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

7 authors at 4 institutions in 1 country.

Maiko OkadaDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Fumiaki OhtakeDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Hiroyuki NishikawaDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Wenwen WuDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Yasushi SaekiDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Keiji TakanaDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Tomohiko OhtaDepartment of Translational Oncology (M.O., W.W., T.O.), Institute of Advanced Medical Science (H.N.), St. Marianna University Graduate School of Medicine, Kawasaki 216-8511, Japan; Institute of Molecular and Cellular Biosciences (M.O.), University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan; Division of Cellular and Molecular Toxicology (F.O.), Biological Safety Research Center, National Institute of Health Sciences, Setagaya-ku, Tokyo 158-8501, Japan; and Laboratory of Protein Metabolism (Y.S., K.T.), Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
St. Marianna University School of Medicine · JPTokyo Metropolitan Institute of Medical Science · JPNational Institute of Health Sciences · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Estrogen receptor (ER)α is a well-characterized ligand-dependent transcription factor. However, the global picture of its nongenomic functions remains to be illustrated. Here, we demonstrate a novel function of ERα during mitosis that facilitates estrogen-dependent cell proliferation. An E3 ubiquitin ligase, UBE3C, was identified in an ERα complex from estrogen-treated MCF-7 breast cancer cells arrested at mitosis. UBE3C interacts with ERα during mitosis in an estrogen-dependent manner. In vitro, estrogen dramatically stimulates the E3 activity of UBE3C in the presence of ERα. This effect was inhibited by the estrogen antagonist tamoxifen. Importantly, estrogen enhances the ubiquitination of cyclin B1 (CCNB1) and destabilizes CCNB1 during mitosis in a manner dependent on endogenous UBE3C. ERα, UBE3C, and CCNB1 colocalize in prophase nuclei and at metaphase spindles before CCNB1 is degraded in anaphase. Depletion of UBE3C attenuates estrogen-dependent cell proliferation without affecting the transactivation function of ERα. Collectively, these results demonstrate a novel ligand-dependent action of ERα that stimulates the activity of an E3 ligase. The mitotic role of estrogen may contribute to its effects on proliferation in addition to its roles in target gene expression.

Indexed as

AnaphaseBreast NeoplasmsCell Line, TumorCell ProliferationCyclin B1Estrogen AntagonistsEstrogen Receptor alphaFemaleHumansMCF-7 CellsMitosisSpindle ApparatusTamoxifenUbiquitinationUbiquitin-Protein LigasesCCNB1 protein, humanCyclin B1Estrogen AntagonistsEstrogen Receptor alphaTamoxifenUBE3C protein, humanUbiquitin-Protein Ligases

Identifiers

PMID26389696
PMCPMC5414673
OpenAlexW1946394036

What OpenQuestion holds

Textmetadata
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.