ArticleWorld journal of gastroenterology2022
Knockdown of DEAD-box 51 inhibits tumor growth of esophageal squamous cell carcinoma
Article in World journal of gastroenterology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 47 citations in OpenAlex.
- The tegument protein VP22 of pseudorabies virus inhibits cGAS condensation by inducing nuclear-to-cytoplasmic translocation of DDX21.PLoS pathogens · 2025Article
- DEAD-box helicase family proteins: emerging targets in digestive system cancers and advances in targeted drug development.Journal of translational medicine · 2024Review
- [Predictive Value of A miRNA Signature for Distant Metastasis in Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024Article
- DDX19A promotes gastric cancer cell proliferation and migration by activating the PI3K/AKT pathway.Cancer cell international · 2024Article
- CSPG4P12 polymorphism served as a susceptibility marker for esophageal cancer in Chinese population.BMC cancer · 2024Article
- IL-1β promotes esophageal squamous cell carcinoma growth and metastasis through FOXO3A by activating the PI3K/AKT pathway.Cell death discovery · 2024Article
- PLCD3 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/P21 signaling.BMC cancer · 2023Article
- The Adipocyte-Macrophage Relationship in Cancer: A Potential Target for Antioxidant Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- DDX1 is a prognostic biomarker and correlates with immune infiltrations in hepatocellular carcinoma.BMC immunology · 2022Article
- RNA interference-mediated silencing of DNA methyltransferase 1 attenuates neuropathic pain by accelerating microglia M2 polarization.BMC neurology · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEsophageal squamous cell carcinoma (ESCC) is one of the most prevalent malignancies that seriously threaten people's health worldwide. DEAD-box helicase 51 (DDX51) is a member of the DEAD-box (DDX) RNA helicase family, and drives or inhibits tumor progression in multiple cancer types.
aimTo determine whether DDX51 affects the biological behavior of ESCC.
methodsThe expression of DDX51 in ESCC tumor tissues and adjacent normal tissues was detected by Immunohistochemistry (IHC) analyses and quantitative PCR (qPCR). We knocked down DDX51 in ESCC cell lines by using a small interfering RNA (siRNA) transfection. The proliferation, apoptosis, and mobility of DDX51 siRNA-transfected cells were detected. The effect of DDX51 on the phosphoinositide 3-kinase (PI3K)/AKT pathway was investigated by western blot analysis. A mouse xenograft model was established to investigate the effects of DDX51 knockdown on ESCC tumor growth.
resultsDDX51 exhibited high expression in ESCC tissues compared with normal tissues and represented a poor prognosis in patients with ESCC. Knockdown of DDX51 induced inhibition of ESCC cell proliferation and promoted apoptosis. Moreover, DDX51 siRNA-expressing cells also exhibited lower migration and invasion rates. Investigations into the underlying mechanisms suggested that DDX51 knockdown induced inactivation of the PI3K/AKT pathway, including decreased phosphorylation levels of phosphate and tensin homolog, PI3K, AKT, and mammalian target of rapamycin. Rescue experiments demonstrated that the AKT activator insulin-like growth factor 1 could reverse the inhibitory effects of DDX51 on ESCC malignant development. Finally, we injected DDX51 siRNA-transfected TE-1 cells into an animal model, which resulted in slower tumor growth.
conclusionOur study suggests for the first time that DDX51 promotes cancer cell proliferation by regulating the PI3K/AKT pathway; thus, DDX51 might be a therapeutic target for ESCC.
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