ArticleMedical oncology (Northwood, London, England)2015
Knockdown of eIF3d inhibits cell proliferation through G2/M phase arrest in non-small cell lung cancer.
Article in Medical oncology (Northwood, London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
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- RNA m7G methylation regulators and targets significantly contribute to chronic obstructive pulmonary disease.Scientific reports · 2025Article
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- Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics.Frontiers in cellular and infection microbiology · 2022Review
- Identification of Hub Genes for Early Diagnosis and Predicting Prognosis in Colon Adenocarcinoma.BioMed research international · 2022Article
- Reduced eIF3d accelerates HIV disease progression by attenuating CD8+ T cell function.Journal of translational medicine · 2019Article
- Overexpression ofDisease markers · 2019Article
- MiR-219-5p suppresses cell proliferation and cell cycle progression in esophageal squamous cell carcinoma by targeting CCNA2.Cellular & molecular biology letters · 2019Article
- Bloom Syndrome Protein Activates AKT and PRAS40 in Prostate Cancer Cells.Oxidative medicine and cellular longevity · 2019Article
- Expression of Concern: Knockdown of eIF3d inhibits cell proliferation through G2/M phase arrest in non-small cell lung cancer.Medical oncology (Northwood, London, England) · 2018Article
- Knockdown of eukaryotic translation initiation factor 3 subunit D (eIF3D) inhibits proliferation of acute myeloid leukemia cells.Molecular and cellular biochemistry · 2018Article
- EIF3B correlates with advanced disease stages and poor prognosis, and it promotes proliferation and inhibits apoptosis in non-small cell lung cancer.Cancer biomarkers : section A of Disease markers · 2018Article
- Proteomics analysis of bladder cancer invasion: Targeting EIF3D for therapeutic intervention.Oncotarget · 2017Article
- Role of Eukaryotic Initiation Factors during Cellular Stress and Cancer Progression.Journal of nucleic acids · 2016Review
- Knockdown of eIF3D inhibits breast cancer cell proliferation and invasion through suppressing the Wnt/β-catenin signaling pathway.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
- Correction · 2019-05-03Error in Text ·
- Expression of concern · 2018-08-18Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Referencing/Attributions ·
- Expression of concern
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) is the most common type of lung cancer and remains the leading cause of cancer-related death worldwide. Eukaryotic translation initiation factor 3, subunit d (eIF3d) has been recognized recently in several human cancers. In this paper, we attempt to evaluate the functional role of eIF3d in NSCLC cells. Lentivirus-mediated RNA interference (RNAi) was applied to silence eIF3d in the human NSCLC cell lines A549 and 95D. Cell viability was measured by MTT. Cell colony-forming ability was measured by colony formation. Cell cycle progression was determined by propidium iodide staining and flow cytometry. Intracellular signaling molecules were detected using a PathScan(®) intracellular signaling array kit. In this study, we firstly proved that lentivirus-mediated RNAi specifically suppressed the expression of eIF3d both at the mRNA and protein levels in A549 and 95D cell lines. Further investigations revealed that eIF3d knockdown significantly inhibited cell proliferation and colony formation. Moreover, the cell cycle of A549 cells was arrested at G2/M phase after eIF3d knockdown. Furthermore, the activations of AKT, HSP27 and SAPK/JNK were suppressed by eIF3d knockdown. This study highlights the crucial role of eIF3d in promoting NSCLC cell proliferation, and provides a foundation for further study into the clinical potential of lentiviral-mediated delivery of eIF3d RNAi therapy for treatment of NSCLC.
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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.