ArticleThe journal of histochemistry and cytochemistry : official journal of the Histochemistry Society2013
DEK depletion negatively regulates Rho/ROCK/MLC pathway in non-small cell lung cancer.
Article in The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Rho-associated kinase (ROCK)-associated proteins and genes-encoded proteins upregulated in lung squamous cell carcinoma (LUSC).Journal of the Egyptian National Cancer Institute · 2026Article
- All hands on DEK: structural insights into a unique histone modifier and chromatin remodeler.Epigenetics & chromatin · 2026Review
- Deficiency of DEK proto-oncogene alleviates allergic rhinitis by inhibiting RhoA/Ezrin-mediated mitochondrial fission.Animal models and experimental medicine · 2025Article
- MLC2: Physiological Functions and Potential Roles in Tumorigenesis.Cell biochemistry and biophysics · 2025Review
- DEK is highly expressed in breast cancer and is associated with malignant phenotype and progression.Oncology letters · 2021Article
- Role of the DEK oncogene in the development of squamous cell carcinoma.International journal of clinical oncology · 2020Review
- DEK Is a Potential Biomarker Associated with Malignant Phenotype in Gastric Cancer Tissues and Plasma.International journal of molecular sciences · 2019Article
- Dek overexpression in murine epithelia increases overt esophageal squamous cell carcinoma incidence.PLoS genetics · 2018Article
- MicroRNA-1292-5p inhibits cell growth, migration and invasion of gastric carcinoma by targeting DEK.American journal of cancer research · 2018Article
- Overexpression of the human DEK oncogene reprograms cellular metabolism and promotes glycolysis.PloS one · 2017Article
- Flavone inhibits migration through DLC1/RhoA pathway by decreasing ROS generation in breast cancer cells.In vitro cellular & developmental biology. Animal · 2016Article
- The DEK oncogene promotes cellular proliferation through paracrine Wnt signaling in Ron receptor-positive breast cancers.Oncogene · 2015Article
- Dissecting the Potential Interplay of DEK Functions in Inflammation and Cancer.Journal of oncology · 2015Review
- High expression of DEK predicts poor prognosis of gastric adenocarcinoma.Diagnostic pathology · 2014Article
- High expression of oncoprotein DEK predicts poor prognosis of small cell lung cancer.International journal of clinical and experimental pathology · 2014Article
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The human DEK proto-oncogene is a nuclear protein with suspected roles in human carcinogenesis. DEK appears to function in several nuclear processes, including transcriptional regulation and modulation of chromatin structure. To investigate the clinicopathological significance of DEK in patients with non-small cell lung cancer (NSCLC), we analyzed DEK immunohistochemistry in 112 NSCLC cases. The results showed that DEK was overexpressed mainly in the nuclear compartment of tumor cells. In squamous cell carcinoma, DEK-positive expression occurred in 47.9% (23/48) of cases, and in lung adenocarcinoma, DEK-positive expression occurred in 67.2% (43/64) of cases and correlated with differentiation, p-TNM stage, and nodal status. Moreover, in lung adenocarcinoma, DEK expression was significantly higher compared with DEK expression in squamous cell carcinoma. Kaplan-Meier analysis showed that patients with low DEK expression had higher overall survival compared with patients with high DEK expression. Depleting DEK expression inhibited cellular proliferation and migration. Furthermore, in DEK-depleted NSCLC cells, we found that RhoA expression was markedly reduced; in conjunction, active RhoA-GTP levels and the downstream effector phosphorylated MLC2 were also reduced. Taken together, DEK depletion inhibited cellular migration in lung cancer cell lines possibly through inactivation of the RhoA/ROCK/MLC signal transduction pathway.
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