ArticleMolecular biology reports2022
PLEK2 promotes the proliferation and migration of non-small cell lung cancer cells in a BRD4-dependent manner.
Article in Molecular biology reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 12 citations in OpenAlex.
- Clinical risk prediction in lung adenocarcinoma using MAL gene and tumor microenvironment features.Discover oncology · 2026Article
- The immune infiltration and prognostic significance of complement and coagulation cascade-related genes in lung adenocarcinoma.Discover oncology · 2025Article
- Pleckstrin-2 promotes the progression of colorectal cancer via YTHDF2-mediated TYMS mRNA stability.Cellular and molecular life sciences : CMLS · 2025Article
- Machine learning‑based construction of damage‑associated molecular patterns related score identifies subtypes of pancreatic adenocarcinoma with distinct prognosis.Oncology letters · 2025Article
- A Screening of Epigenetic Therapeutic Targets for Non-Small Cell Lung Cancer Reveals PADI4 and KDM6B as Promising Candidates.International journal of molecular sciences · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIt has been reported that Pleckstrin 2 (PLEK2) acts as an oncogene in non-small cell lung cancer (NSCLC). Bromodomain containing protein 4 (BRD4), an important transcriptional regulator of tumorigenesis, has been shown to play a key role in NSCLC. However, whether BRD4 regulates the transcription of PLEK2 and further promotes the proliferation and migration of NSCLC remains unknown. METHODS AND
resultsIn this study, we performed western blotting, real-time quantitative polymerase chain reaction, immunofluorescence, cell scratch wound assay and chromatin immunoprecipitation. According to these results, we found that PLEK2 plays a tumor‑promoting role in NSCLC via the PI3K/AKT signaling pathway. Moreover, BRD4 expression is significantly upregulated in NSCLC cell lines and suppression of BRD4 expression by siBRD4 and JQ-1 inhibits NSCLC cell lines proliferation and migration. Prominently, we first confirmed that BRD4 binds to the promoter region of the PLEK2 gene, which explains the mechanism by which BRD4 regulates the transcription of PLEK2 gene from the perspective of epigenetics.
conclusionsThe present study suggested that PLEK2 promotes the proliferation and migration of NSCLC in a BRD4-dependent manner and provided key insights into the potential avenues for preventing and treating NSCLC.
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