Evidence map›Paper›PMID 29445107›Full record

ArticleScientific reports2018

Progesterone Receptor Membrane Component 1 suppresses the p53 and Wnt/β-catenin pathways to promote human pluripotent stem cell self-renewal.

Ji Yea Kim, So Young Kim, Hong Seo Choi, Min Kyu Kim, Hyun Min Lee, Young-Joo Jang, Chun Jeih Ryu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 43 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

7 authors at 2 institutions in 1 country.

Ji Yea KimDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea.
So Young KimDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea.
Hong Seo ChoiDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea.
Min Kyu KimDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea.
Hyun Min LeeDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea.
Young-Joo JangDepartment of Nanobiomedical Science, BK21 PLUS Global Research Center for Regenerative Medicine, Dankook University, Cheonan, Korea. yjjang@dankook.ac.kr.
Chun Jeih RyuDepartment of Integrative Bioscience and Biotechnology, Institute of Anticancer Medicine Development, Sejong University, Seoul, Korea. cjryu@sejong.ac.kr.
Sejong University · KRDankook University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Progesterone receptor membrane component 1 (PGRMC1) is a multifunctional heme-binding protein involved in various diseases, including cancers and Alzheimer's disease. Previously, we generated two monoclonal antibodies (MAbs) 108-B6 and 4A68 against surface molecules on human pluripotent stem cells (hPSCs). Here we show that PGRMC1 is the target antigen of both MAbs, and is predominantly expressed on hPSCs and some cancer cells. PGRMC1 is rapidly downregulated during early differentiation of hPSCs. Although PGRMC1 knockdown leads to a spread-out morphology and impaired self-renewal in hPSCs, PGRMC1 knockdown hPSCs do not show apoptosis and autophagy. Instead, PGRMC1 knockdown leads to differentiation of hPSCs into multiple lineage cells without affecting the expression of pluripotency markers. PGRMC1 knockdown increases cyclin D1 expression and decreases Plk1 expression in hPSCs. PGRMC1 knockdown also induces p53 expression and stability, suggesting that PGRMC1 maintains hPSC self-renewal through suppression of p53-dependent pathway. Analysis of signaling molecules further reveals that PGRMC1 knockdown promotes inhibitory phosphorylation of GSK-3β and increased expression of Wnt3a and β-catenin, which leads to activation of Wnt/β-catenin signaling. The results suggest that PGRMC1 suppresses the p53 and Wnt/β-catenin pathways to promote self-renewal and inhibit early differentiation in hPSCs.

Indexed as

Apoptosisbeta CateninCell DifferentiationCell LineageCell ProliferationCell Self RenewalDown-RegulationGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHuman Embryonic Stem CellsHumansMembrane ProteinsPhosphorylationPluripotent Stem CellsReceptors, Progesteronebeta CateninCTNNB1 protein, humanGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMembrane ProteinsPGRMC1 protein, humanReceptors, ProgesteroneTP53 protein, humanTranscription FactorsTumor Suppressor Protein p53Wnt3A ProteinWNT3A protein, human

Identifiers

PMID29445107
PMCPMC5813096
OpenAlexW2806181774

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.