ArticleHistology and histopathology2020
Knockdown of ADAMDEC1 inhibits the progression of glioma in vitro.
Article in Histology and histopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- ADAMDEC1 predicts prognosis and immunotherapy response in a pan-cancer study with experimental validation.Discover oncology · 2026Article
- ADAMDEC1 promotes cervical squamous cell carcinoma by enhancing the JAK/STAT signaling pathway through modulation of TYMP.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- ADAMDEC1 promotes the malignant progression of cholangiocarcinoma by regulating NF-κB signaling pathway.Scientific reports · 2025Article
- An immune signature to predict the prognosis ofAging · 2023Article
- Article
- Potential biomarkers that discriminate rheumatoid arthritis and osteoarthritis based on the analysis and validation of datasets.BMC musculoskeletal disorders · 2022Article
- Upregulation of ADAMDEC1 correlates with tumor progression and predicts poor prognosis in non-small cell lung cancer (NSCLC) via the PI3K/AKT pathway.Thoracic cancer · 2022Article
- ADAMDEC1 accelerates GBM progressionFrontiers in oncology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundGlioma is one of the most lethal malignant tumors all over the world. The prognosis of patients with high‑grade glioma remains very poor. Therefore, it is urgent to find a novel strategy for the treatment of glioma. It has been reported that ADAMDEC1 could regulate the progression of multiple diseases, including cancers. However, the role of ADAMDEC1 during the tumorigenesis of glioma remains largely unknown. Methods, Gene expression of ADAMDEC1 in glioma tissues or in cells was detected by qRT-PCR. Western blot was performed to measure the protein expressions of p53, active caspase3, active caspase9, CDK2 and Cyclin A in glioma cells. Cell proliferation was detected by CCK-8 assay. Cell apoptosis or cycle was tested by flow cytometry. Transwell was used to test the invasion of glioma cells.
resultsThe expression of ADAMDEC1 in glioma tissues or cells was significantly upregulated. In addition, downregulation of ADAMDEC1 notably inhibited the proliferation and induced apoptosis of glioma cells through upregulation of active caspase 3 and active caspase 9. Besides, silencing of ADAMDEC1 obviously induced G1 arrest in glioma cells via modulation of cell cycle-related proteins. Finally, knockdown of ADAMDEC1 significantly inhibited the migration and invasion of glioma cells. In contrast, overexpression of ADAMDEC1 promoted cell proliferation, migration and invasion of glioma cells.
conclusionDownregulation of ADAMDEC1 could significantly inhibit the tumorigenesis of glioma in vitro, which may serve as a novel target for the treatment of glioma.
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