ArticleLasers in medical science2019
AMPH-1 is a tumor suppressor of lung cancer by inhibiting Ras-Raf-MEK-ERK signal pathway.
Article in Lasers in medical science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 14 citations in OpenAlex.
- GATOR1 complex controls cisplatin sensitivity.Cell death & disease · 2025Article
- GPER1 is involved in shaping tumor immune microenvironment and its expression is decreased in NSCLC tumorigenesis.Scientific reports · 2025Article
- Genetic Factors Related to the Development or Progression of Mesoamerican Endemic Nephropathy.International journal of molecular sciences · 2025Review
- Transcriptome sequencing reveals novel molecular features of SLE severity.Frontiers in genetics · 2023Article
- Review
- AMPH1 functions as a tumour suppressor in ovarian cancer via the inactivation of PI3K/AKT pathway.Journal of cellular and molecular medicine · 2020Article
- Silencing ARAF Suppresses the Malignant Phenotypes of Gallbladder Cancer Cells.BioMed research international · 2020Article
- AMPH-1 As A Critical Tumor Suppressor That Inhibits Osteosarcoma Progression.Cancer management and research · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amphiphysin 1 (AMPH-1) is a nerve terminal-enriched protein and it is a 128-kD protein with three identified functional domains. Some studies found that AMPH-1 was a dominant autoantigen associated with breast cancer and melanoma. However, its function in lung cancer is unknown. Here, we showed that AMPH-1 knockdown dramatically increased cell proliferation, attenuated cell apoptosis, and promoted cell cycle progression in human lung cancer cells. In vivo xenograft studies confirmed that the AMPH-1-knockdown cells were more tumorigenic than the controls. Moreover, we demonstrated that silencing AMPH-1 markedly activated Ras-Raf-MEK-ERK signal pathway. In summary, our results identified the anti-oncogenic function of AMPH-1 in lung cancer in vitro and in vivo. It is proposed that AMPH-1 may have potential as a new therapeutic target in human lung cancer treatment.
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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.