Identification of Key Transcription Factors Associated with Lung Squamous Cell Carcinoma

Zhang, Feng; Chen, Xia; Wei, Ke; Liu, Daoming; Xu, Xiaodong; Zhang, Xing; Shi, Hong

doi:10.12659/msm.898297

Cited by 27 publications

(22 citation statements)

References 39 publications

(40 reference statements)

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“…More recent studies revealed that the DNA-binding capability of RDM1 is enhanced at low pH, indicating that it may function in acidic conditions such as the tumor microenvironment (17). Furthermore, RDM1 has been shown to be upregulated at the mRNA level in lung squamous cell carcinoma (18). Nonetheless, despite the growing evidence, the precise function of RDM1 in NSCLC remains largely unknown.…”

Section: Introductionmentioning

confidence: 99%

RAD52 motif‑containing protein�1 promotes non‑small cell lung cancer cell proliferation and survival via cell cycle regulation

Wang

et al. 2018

Oncol Rep

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DNA repair proteins such as RAD52 have been implicated in tumor progression and response to chemotherapy. RAD52 motif‑containing protein 1 (RDM1) has been implicated in the response to chemotherapeutic agent cisplatin; however, its function in lung cancer progression remains unclear. This study aimed to investigate the role of RDM1 in the progression of non‑small cell lung cancer (NSCLC). We found elevated RDM1 mRNA and protein expression in NSCLC tissues and cell lines compared to levels in normal lung cells. RDM1 protein expression in lung cancer tissues was found to correlate with tumor size, histological differentiation, lymph node metastasis and tumor‑node‑metastasis (TNM) stage. Knockdown of the RDM1 gene with siRNA significantly reduced the cellular proliferation rate and increased apoptosis in the human NSCLC cell line, NCI‑H1299. Compared to wild‑type NCI‑H1299 cells, RDM1 knockdown enhanced the activity of caspase‑3 and caspase‑7, and decreased the proportion of cells in the S‑phase of the cell cycle. Taken together, these data imply that RDM1 promotes the survival and proliferation of NSCLC cells. Due to its similarity to RAD52, we hypothesized that RDM1 potentially repairs DNA double‑strand breaks arising through DNA replication, thereby preventing G2/M cell cycle arrest. Accordingly, specific targeting of RDM1 may be a novel therapeutic strategy in the treatment of NSCLC.

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Section: Introductionmentioning

confidence: 99%

RAD52 motif‑containing protein�1 promotes non‑small cell lung cancer cell proliferation and survival via cell cycle regulation

Wang

et al. 2018

Oncol Rep

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“…SCLC is another more aggressive form of LC, and the 5-year overall survival of SCLC patients is only about 5% [ 3 – 6 ]. With advances in pathologic and molecular studies of LC, early detection, diagnosis, and treatment are of great significance for the management of LC [ 7 , 8 ]. Hence, identification of molecules that are correlated with the clinical features of LC patients might be helpful in the management of LC.…”

Section: Introductionmentioning

confidence: 99%

Correlations Between mRNA Levels of Centrosomal Protein 55 (CEP55) and Clinical Features of Patients with Lung Cancer

Zhang

Bu-qiang

et al. 2018

Med Sci Monit

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BackgroundThe aim of this study was to investigate the prognostic relevance of CEP55 in lung cancer (LC).Material/MethodsLC microarray profile GSE30219 was obtained from the GEO database. The 2-sample t test was performed to clarify the difference in CEP55 expression between LC and normal lung tissue. The chi-square test and logistic regression analysis were preformed to investigate the relationship between CEP55 expression and the clinical features of LC patients. Log-rank test and Cox proportional hazards regression analysis were conducted to evaluate the disease-free survival (DFS) and overall survival (OS) of LC patients. Gene set enrichment analysis was conducted to investigate the related mechanisms.ResultsCEP55 was significantly increased in LC cells relative to normal lung tissues (P<0.0001). Univariate and multivariate correlation analyses demonstrated that CEP55 expression was associated with advanced T and N staging of LC (P<0.0001). Survival analyses indicated that CEP55 expression was an independent risk factor for DFS (HR: 1.515, 95% CI: 1.277–1.797, P<0.0001) and OS (HR: 1.436, 95% CI: 1.278–1.615). CEP55 might affect the proliferation of LC cells through Myc signaling, DNA repair, and G2M checkpoint.ConclusionsOur results indicated that CEP55 was increased in LC cells and was associated with poor clinical outcomes of LC patients, and could be a prognostic biomarker for LC.

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“…Additionally, the polymorphism of P73 is suggested to be highly associated with susceptibility to smoking‐related lung cancer . Moreover, transcription factors (TFs) have been identified in lung SCC . In spite of these findings, lung cancer prognosis in clinical practice has not improved.…”

Section: Introductionmentioning

confidence: 99%

“…6 Moreover, transcription factors (TFs) have been identified in lung SCC. 7 In spite of these findings, lung cancer prognosis in clinical practice has not improved. Currently, there are no identified molecular targets for therapy of smoking-related lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

Sun

Miao

et al. 2017

Thoracic Cancer

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BackgroundCigarette smoking is one of the greatest preventable risk factors for developing cancer, and most cases of lung squamous cell carcinoma (lung SCC) are associated with smoking. The pathogenesis mechanism of tumor progress is unclear. This study aimed to identify biomarkers in smoking‐related lung cancer, including protein‐coding gene, long noncoding RNA, and transcription factors.MethodsWe selected and obtained messenger RNA microarray datasets and clinical data from the Gene Expression Omnibus database to identify gene expression altered by cigarette smoking. Integrated bioinformatic analysis was used to clarify biological functions of the identified genes, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, the construction of a protein–protein interaction network, transcription factor, and statistical analyses. Subsequent quantitative real‐time PCR was utilized to verify these bioinformatic analyses.ResultsFive hundred and ninety‐eight differentially expressed genes and 21 long noncoding RNA were identified in smoking‐related lung SCC. GO and KEGG pathway analysis showed that identified genes were enriched in the cancer‐related functions and pathways. The protein–protein interaction network revealed seven hub genes identified in lung SCC. Several transcription factors and their binding sites were predicted. The results of real‐time quantitative PCR revealed that AURKA and BIRC5 were significantly upregulated and LINC00094 was downregulated in the tumor tissues of smoking patients. Further statistical analysis indicated that dysregulation of AURKA, BIRC5, and LINC00094 indicated poor prognosis in lung SCC.ConclusionProtein‐coding genes AURKA, BIRC5, and LINC00094 could be biomarkers or therapeutic targets for smoking‐related lung SCC.

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Identification of Key Transcription Factors Associated with Lung Squamous Cell Carcinoma

Cited by 27 publications

References 39 publications

RAD52 motif‑containing protein�1 promotes non‑small cell lung cancer cell proliferation and survival via cell cycle regulation

RAD52 motif‑containing protein�1 promotes non‑small cell lung cancer cell proliferation and survival via cell cycle regulation

Correlations Between mRNA Levels of Centrosomal Protein 55 (CEP55) and Clinical Features of Patients with Lung Cancer

Differential protein‐coding gene and long noncoding RNA expression in smoking‐related lung squamous cell carcinoma

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