Evidence map›Paper›PMID 32704174›Full record

ArticleBritish journal of cancer2020

Progesterone receptor membrane component 1 promotes the growth of breast cancers by altering the phosphoproteome and augmenting EGFR/PI3K/AKT signalling.

Diego A Pedroza, Venkatesh Rajamanickam, Ramadevi Subramani, Alejandra Bencomo, Adriana Galvez, Rajkumar Lakshmanaswamy

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 58 citations in OpenAlex.

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  13. Sigma Receptors: Novel Regulators of Iron/Heme Homeostasis and Ferroptosis.International journal of molecular sciences · 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

6 authors at 2 institutions in 1 country.

Diego A PedrozaGraduate School of Biomedical Sciences, Texas Tech University Health Sciences Center El Paso, El Paso, TX, 79905, USA.
Venkatesh RajamanickamEarle A. Chiles Research Institute, Providence Cancer Institute, Portland, OR, 97213, USA.
Ramadevi SubramaniGraduate School of Biomedical Sciences, Texas Tech University Health Sciences Center El Paso, El Paso, TX, 79905, USA.
Alejandra BencomoDepartment of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX, 79905, USA.
Adriana GalvezDepartment of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso, El Paso, TX, 79905, USA.
Rajkumar LakshmanaswamyGraduate School of Biomedical Sciences, Texas Tech University Health Sciences Center El Paso, El Paso, TX, 79905, USA. rajkumar.lakshmanaswamy@ttuhsc.edu.ORCID http://orcid.org/0000-0001-7825-8122
Texas Tech University · USProvidence Portland Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased expression of the progesterone receptor membrane component 1 (PGRMC1) has been linked to multiple cancers, including breast cancer. Despite being a regulatory receptor and a potential therapeutic target, the oncogenic potential of PGRMC1 has not been studied.

methodsThe impact of PGRMC1 on breast cancer growth and progression was studied following chemical inhibition and alteration of PGRMC1 expression, and evaluated by using online-based gene expression datasets of human breast cancer tissue. MTS, flow cytometry, qPCR, Western blotting, confocal microscopy and phosphoproteome analysis were performed.

resultsWe observed higher PGRMC1 levels in both ER-positive ZR-75-1 and TNBC MDA-MB-468 cells. Both chemical inhibition and silencing decreased cell proliferation, induced cell-cycle arrest, promoted apoptosis and reduced the migratory and invasive capabilities of ZR-75-1 and MDA-MB-468 cells. Further, phosphoproteome analysis demonstrated an overall decrease in activation of proteins involved in PI3K/AKT/mTOR and EGFR signalling pathways. In contrast, overexpression of PGRMC1 in non-malignant MCF10A cells resulted in increased cell proliferation, and enhanced activity of PI3K/AKT/mTOR and EGFR signalling pathways.

conclusionsOur data demonstrate that PGRMC1 plays a prominent role in regulating the growth of cancer cells by altering the PI3K/AKT/mTOR and EGFR signalling mechanisms in both ER-positive and TNBC cells.

Indexed as

ProteomeBreast NeoplasmsCell Line, TumorCell ProliferationErbB ReceptorsFemaleHumansMembrane ProteinsPhosphatidylinositol 3-KinasesPhosphoproteinsProto-Oncogene Proteins c-aktReceptors, ProgesteroneSignal TransductionTOR Serine-Threonine KinasesEGFR protein, humanErbB ReceptorsMembrane ProteinsMTOR protein, humanPGRMC1 protein, humanPhosphatidylinositol 3-KinasesPhosphoproteinsProteomeProto-Oncogene Proteins c-aktReceptors, ProgesteroneTOR Serine-Threonine Kinases

Identifiers

PMID32704174
PMCPMC7553958
OpenAlexW3044873414

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.