Evidence map›Paper›PMID 33122470›Full record

ArticleInternational journal of stem cells2021

Inhibition of MUC1-C Increases ROS and Cell Death in Mouse Embryonic Stem Cells.

Jeong-A Park, Sangkyu Park, Jun-Kyu Choi, Myung-Kwan Han, Younghee Lee

Open access · diamondAbstract read
In one paragraph

Article in International journal of stem cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Frontiers in pharmacology · 2024
    Article
  3. Article
  4. Review
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 2 institutions in 1 country.

Jeong-A ParkDepartment of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, Korea.
Sangkyu ParkDepartment of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, Korea.
Jun-Kyu ChoiDepartment of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, Korea.
Myung-Kwan HanDepartment of Microbiology, Chonbuk National University Medical School, Jeonju, Korea.
Younghee LeeDepartment of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, Korea.
Chungbuk National University · KRJeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesEmbryonic stem (ES) cells have the capacity to self-renew and generate all types of cells. MUC1-C, a cytoplasmic subunit of MUC1, is overexpressed in various carcinomas and mediates signaling pathways to regulate intracellular metabolic processes and gene expression involved in the maintenance of cancer cells. However, the functional role of MUC1-C in ES cells is not well understood. In this study, we investigated the role of MUC1-C on growth, survival, and differentiation of mouse ES (mES) cells. METHODS AND

resultsUndifferentiated mES cells expressed the MUC1-C protein and the expression level was decreased during differentiation. Inhibition of MUC1-C, by the specific inhibitor GO201, reduced proliferation of mES cells. However, there was no prominent effect on pluripotent markers such as Oct4 expression and STAT3 signaling, and MUC1-C inhibition did not induce differentiation. Inhibition of MUC1-C increased the G1 phase population, decreased the S phase population, and increased cell death. Furthermore, inhibition of MUC1-C induced disruption of the ROS balance in mES cells.

conclusionsThese results suggest that MUC1-C is involved in the growth and survival of mES cells.

Indexed as

Cell cycleMouse embryonic stem cellsMUC1-CProliferationROS

Identifiers

PMID33122470
PMCPMC8138657
OpenAlexW3095765269

What OpenQuestion holds

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LicenceCC BY-NC
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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.