Overexpression of CD88 predicts poor prognosis in non-small-cell lung cancer

Gu, Jie; Ding, Jianyong; Chen, Lu; Zhang, Lin; Chu, Yiwei; Zhao, Guochao; Guo, Jìng; Ge, Di

doi:10.1016/j.lungcan.2013.04.020

Cited by 73 publications

(81 citation statements)

References 37 publications

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“…Tissue microarrays were constructed as described in a previous study (21). Digoxin (DIG)-labeled oligonucleotide probes complementary to hsa-miR-126 were designed as previously described and purchased from ExonBIO (22).…”

Section: Tissue Microarray and In Situ Hybridizationmentioning

confidence: 99%

DNMT1–MicroRNA126 Epigenetic Circuit Contributes to Esophageal Squamous Cell Carcinoma Growth via ADAM9–EGFR–AKT Signaling

Liu

Jiang

et al. 2015

Clinical Cancer Research

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100

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Purpose: MicroRNAs (miRNA) are involved in and are controlled by epigenetic regulation, and thereby form a reciprocal regulatory circuit. Using next-generation sequencing (NGS)-based miRNA profiling, this study aimed to discover esophageal squamous cell carcinoma (ESCC)-specific miRNAs and miRNArelated epigenetic modulations.Experimental Design: NGS-based miRNA profiles were generated for four pairs of ESCC tissues and adjacent normal tissues. In situ hybridization was used to assess miRNA expression and its correlation with prognosis. miRNA-related DNA methylations were identified using bisulfite genomic sequencing, and the role of DNA methyltransferase 1 (DNMT1) was investigated using RNA interference. miRNA targets were screened by mRNA sequencing, and functional validation was performed in vitro and in vivo.Results: NGS-based miRNA profiling identified 78 differentially expressed miRNAs in ESCC. Among them, microRNA126-3p (miR-126) was significantly downregulated, and its downregulation correlated with poor ESCC prognosis. Downregulation of miR-126 was due to promoter hypermethylation of its host gene, Egfl7. DNMT1 was aberrantly upregulated in ESCC and responsible for the hypermethylation of Egfl7. Intriguingly, DNMT1 was suppressed by overexpression of miR-126, indicating the existence of a regulatory feedback circuit. ADAM9 was identified as a key target of miR-126. Ectopic expression of miR-126 or silencing of ADAM9 reduced ESCC cell proliferation and migration by inhibiting epidermal growth factor receptor-AKT signaling.Conclusions: Our results indicate that miR-126 is a potential prognostic indicator for ESCC and suggest that a novel "DNMT1-miR-126 epigenetic circuit" is involved in ESCC progression. Consequently, miR-126-based epigenetic modulations may provide a basic rationale for new approaches to antitumor therapeutics.

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Section: Tissue Microarray and In Situ Hybridizationmentioning

confidence: 99%

DNMT1–MicroRNA126 Epigenetic Circuit Contributes to Esophageal Squamous Cell Carcinoma Growth via ADAM9–EGFR–AKT Signaling

Liu

Jiang

et al. 2015

Clinical Cancer Research

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100

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“…47 It is reported that cancers with overexpression of C5aR are considered aggressive and have poor prognosis. 48,49 In 2012, Corrales et al 50 found that the lung cancer cells could produce C5a and high amount of C5a was detected in the patients with NSCLC. C5aR blockade contributed to the reduction of MDSC and inhibited tumor growth.…”

Section: Combination Strategiesmentioning

confidence: 99%

Management of Italian Patients With Advanced Non–Small-Cell Lung Cancer After Second-Line Treatment: Results of the Longitudinal Phase of the LIFE Observational Study

Marinis

Ardizzoni

Fontanini

et al. 2014

Clinical Lung Cancer

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“…As a transmembrane growth factor receptor, EGFR exhibits tyrosine kinase activity, which is important for its involvement in controlling the survival and proliferation of cells (28), and it has been indicated that the expression of EGFR was negatively associated with the apoptosis of cancer cells (29). Various mechanisms, including gene mutation, copy number variation, and protein overexpression are associated with the deregulation of cellular activity of EGFR (30,31).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-27b reverses docetaxel resistance of non-small cell lung carcinoma cells via targeting epithelial growth factor receptor

Chen

Wang

Zhou

et al. 2016

Molecular Medicine Reports

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Abstract. MicroRNA (miR)-27b has been reported to partici pate in regulating the activity of non-small cell lung carcinoma (NSCLC) cells. Additionally, when downregulated in NSCLC it promotes resistance to docetaxel; however, the underlying molecular mechanism remains largely unknown. Using reverse transcription-quantitative polymerase chain reaction, the present study determined that the expression of miR-27b was significantly reduced in NSCLC cells that were resistant to docetaxel. In addition, epidermal growth factor receptor (EGFR) was identified as a possible target of miR-27b by searching the online miRNA database, TargetScan.

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Overexpression of CD88 predicts poor prognosis in non-small-cell lung cancer

Cited by 73 publications

References 37 publications

DNMT1–MicroRNA126 Epigenetic Circuit Contributes to Esophageal Squamous Cell Carcinoma Growth via ADAM9–EGFR–AKT Signaling

DNMT1–MicroRNA126 Epigenetic Circuit Contributes to Esophageal Squamous Cell Carcinoma Growth via ADAM9–EGFR–AKT Signaling

Management of Italian Patients With Advanced Non–Small-Cell Lung Cancer After Second-Line Treatment: Results of the Longitudinal Phase of the LIFE Observational Study

MicroRNA-27b reverses docetaxel resistance of non-small cell lung carcinoma cells via targeting epithelial growth factor receptor

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