ArticleMolecular medicine reports2020
DDX46 silencing inhibits cell proliferation by activating apoptosis and autophagy in cutaneous squamous cell carcinoma.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Comprehensive analysis indicates DDX46 as a novel biomarker for the prognosis of lung adenocarcinoma.Oncology letters · 2025Article
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- DDX3X dynamics, glioblastoma's genetic landscape, therapeutic advances, and autophagic interplay.Medical oncology (Northwood, London, England) · 2024Review
- PRR14 acts a novel oncogene activating the PI3K signal pathway in human cutaneous squamous cell carcinoma.Journal of Cancer · 2023Article
- Seed sequence polymorphism rs2168518 and allele-specific target gene regulation of hsa-miR-4513.Human molecular genetics · 2022Article
- Role of AUF1 in modulating the proliferation, migration and senescence of skin cells.Experimental and therapeutic medicine · 2022Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DEAD‑Box Helicase 46 (DDX46) is an ATP‑dependent RNA helicase that plays a central role in transcription splicing and ribosome assembly. However, the role of DDX46 in cutaneous squamous cell carcinoma (CSCC) remains to be elucidated. The aim of the present study was to investigate the role of DDX46 in CSCC by assessing DDX46 expression levels in CSCC tissues and cell lines. The effect of DDX46 silencing on CSCC cell proliferation, apoptosis and autophagy were also analyzed. It was demonstrated that DDX46 was significantly overexpressed in CSCC tissues and cells (P<0.05). Furthermore, it was found that DDX46 silencing could dramatically inhibit cell proliferation (P<0.05). Moreover, cell apoptosis and autophagy were activated in DDX46 silencing groups (P<0.05). Therefore, the present results suggested that DDX46 was overexpressed in CSCC and that DDX46 silencing can inhibit cell proliferation by inducing apoptosis and activating autophagy. Thus, DDX46 may serve as a novel potential therapeutic target for CSCC.
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