ArticleBioscience reports2017
Dysregulation of POPDC1 promotes breast cancer cell migration and proliferation.
Article in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- DNA hypermethylation drives BVES-mediated autophagy to promote cisplatin resistance in lung adenocarcinoma.Journal of bioenergetics and biomembranes · 2026Article
- Dual Biological Effects and Mechanisms of Gut Microbiota in Breast Cancer: A Review.Current pharmaceutical biotechnology · 2026Review
- Systemic AAV9.BVES delivery ameliorates muscular dystrophy in a mouse model of LGMDR25.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Modulation of POPDC1 Expression by Phenothiazine and Trifluoperazine Suppress Colon Cancer Growth and Migration.Asian Pacific journal of cancer prevention : APJCP · 2022Article
- The Transition from Gastric Intestinal Metaplasia to Gastric Cancer InvolvesInternational journal of molecular sciences · 2021Article
- Review
- Selective small-molecule EPAC activators.Biochemical Society transactions · 2019Review
- The Popeye domain containing gene family encoding a family of cAMP-effector proteins with important functions in striated muscle and beyond.Journal of muscle research and cell motility · 2019Review
- Ten years of research on the role of BVES/ POPDC1 in human disease: a review.OncoTargets and therapy · 2019Review
- Blood Vessel Epicardial Substance (BVES) in junctional signaling and cancer.Tissue barriers · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer subtypes such as triple-negative that lack the expression of oestrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor 2 receptor (HER2), remain poorly clinically managed due to a lack of therapeutic targets. This necessitates identification and validation of novel targets. Suppression of Popeye domain-containing protein 1 (POPDC1) is known to promote tumorigenesis and correlate to poor clinical outcomes in various cancers, and also promotes cardiac and skeletal muscle pathologies. It remains to be established whether POPDC1 is dysregulated in breast cancer, and whether overcoming the dysregulation of POPDC1 could present a potential therapeutic strategy to inhibit breast tumorigenesis. We assessed the potential of POPDC1 as a novel target for inhibiting breast cancer cell migration and proliferation. POPDC1 was significantly suppressed with reduced cell membrane localization in breast cancer cells. Furthermore, functional suppression of POPDC1 promoted breast cancer cell migration and proliferation, which were inhibited by POPDC1 overexpression. Finally, cAMP interacts with POPDC1 and up-regulates its expression in breast cancer cells. These findings suggest that POPDC1 plays a role in breast tumorigenesis and represents a potential therapeutic target or biomarker in breast cancer medicine.
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Registered trials
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.