Evidence map›Paper›PMID 36769125›Full record

ArticleInternational journal of molecular sciences2023

The Orphan GPR50 Receptor Regulates the Aggressiveness of Breast Cancer Stem-like Cells via Targeting the NF-kB Signaling Pathway.

Polash Kumar Biswas, Sang Rok Park, Jongyub An, Kyung Min Lim, Ahmed Abdal Dayem, Kwonwoo Song, Hye Yeon Choi, Yujin Choi, Kyoung Sik Park, Hyun Jin Shin and 4 more

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
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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

14 authors.

Polash Kumar BiswasDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Sang Rok ParkDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Jongyub AnDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Kyung Min LimDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.ORCID 0000-0001-5456-255X
Ahmed Abdal DayemDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.ORCID 0000-0003-3873-9903
Kwonwoo SongDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.ORCID 0000-0001-9150-4754
Hye Yeon ChoiDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Yujin ChoiDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Kyoung Sik ParkDepartment of Surgery, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul 05029, Republic of Korea.ORCID 0000-0001-9806-9839
Hyun Jin ShinDepartment of Ophthalmology, Research Institute of Medical Science, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul 05029, Republic of Korea.
Aram KimDepartment of Urology, Konkuk University Medical Center, Konkuk University School of Medicine, Seoul 05029, Republic of Korea.
Minchan GilDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.
Subbroto Kumar SahaDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.ORCID 0000-0003-1325-3499
Ssang-Goo ChoDepartment of Stem Cell and Regenerative Biotechnology, Molecular & Cellular Reprogramming Center (MCRC), Incurable Disease Animal Model & Stem Cell Institute (IDASI), Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea.ORCID 0000-0002-0968-7932

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The expression of GPR50 in CSLC and several breast cancer cell lines was assessed by RT-PCR and online platform (UALCAN, GEPIA, and R2 gene analysis). The role of GPR50 in driving CSLC, sphere formation, cell proliferation, and migration was performed using shGPR50 gene knockdown, and the role of GPR50-regulated signaling pathways was examined by Western blotting and Luciferase Assay. Herein, we confirmed that the expression of G protein-coupled receptor 50 (GPR50) in cancer stem-like cells (CSLC) is higher than that in other cancer cells. We examined that the knockdown of GPR50 in CSLC led to decreased cancer properties, such as sphere formation, cell proliferation, migration, and stemness. GPR50 silencing downregulates NF-kB signaling, which is involved in sphere formation and aggressiveness of CSLC. In addition, we demonstrated that GPR50 also regulates ADAM-17 activity by activating NOTCH signaling pathways through the AKT/SP1 axis in CSLC. Overall, we demonstrated a novel GPR50-mediated regulation of the NF-κB-Notch signaling pathway, which can provide insights into CSLC progression and prognosis, and NF-κB-NOTCH-based CSLC treatment strategies.

Indexed as

Breast NeoplasmsNF-kappa BCell Line, TumorFemaleHumansNerve Tissue ProteinsReceptors, G-Protein-CoupledSignal TransductionGPR50 protein, humanNerve Tissue ProteinsNF-kappa BReceptors, G-Protein-CoupledADAM17breast cancer stem cell (BCSC)GPR50NF-kBNotch

Identifiers

PMID36769125
PMCPMC9917945

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Registered trials

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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.