Do Esophageal Squamous Cell Carcinoma Patients Have an Increased Risk of Coexisting Colorectal Neoplasms?

Jang, Byung Ik; Hwang, Moon Joo

doi:10.5009/gnl15564

Cited by 2 publications

(2 citation statements)

References 10 publications

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“…The incidence and mortality rate of human lung cancer has been growing rapidly in recent years and is one of the most threatening types of malignant tumors to health and survival ( 28 ). NSCLC represents more than 85% of lung cancer cases according to statistical clinical data ( 29 ).…”

Section: Discussionmentioning

confidence: 99%

Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer

Yuan

Lin

et al. 2018

Exp Ther Med

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Non-small cell lung cancer (NSCLC) is the most frequent type of human lung cancer; lung cancer is responsible for the highest rates of cancer-associated mortality in the world. Cysteine-rich angiogenic inducer-61 (CYR-61) has been identified as a tumorigenesis-, development- and metastasis-related gene, and is reported to enhance proliferation, migration and invasion through hepatocyte growth factor (HGF)-induced scattering and the metastasis-inducing HGF/Met signaling pathway in tumor cells and xenograft models. CYR-61 is a protein that promotes human lung cancer cell metastasis and is closely related to the patient's prognosis in NSCLC. The purpose of the present study was to investigate whether CYR-61 may serve as a dual potential target for gene therapy of human NSCLC. In the present study, an antibody targeted against CYR-61 (anti-CYR-61) was constructed and the therapeutic effects and underlying mechanism of this antibody in NSCLC cells and mice with NSCLC was investigated. It was observed that NSCLC cell viability, migration and invasion were inhibited while cell apoptosis was induced by the neutralization of CYR-61 protein by anti-CYR-61. Western blotting demonstrated that extracellular signal-regulated kinase (ERK) and protein kinase B (AKT) expression levels in NSCLC cells were decreased following treatment with anti-CYR-61. In addition, it was observed that inhibition of NSCLC cell viability was achieved by the suppression of the epithelial-mesenchymal transition signaling pathway. ERK and AKT phosphorylation levels were downregulated in NSCLC cells and tumors following anti-CYR-61 treatment. Analysis of a murine model indicated that tumor growth was inhibited and tumor metastasis was significantly suppressed (P<0.01) following anti-CYR-61 treatment for CYR-61. In conclusion, CYR-61 may serve as a potential target for gene therapy for the treatment of human NSCLC.

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Section: Discussionmentioning

confidence: 99%

Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer

Yuan

Lin

et al. 2018

Exp Ther Med

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“…EC-109 and Het-1A cells were lysed and used to analyzed Grim-19 protein expression, according to a previous study (29). For immunostaining, EC-109 cells (1x10 6 ) pre-treated with PBS, rAd or rAd-Grim-19 for 24 h, or tumors from esophageal carcinoma xenograph mice in PBS, rAd and rAd-Grim-19 groups on day 30 were fixed using 10% for maldehyde for 15 min at room temperature and embedded in paraffin.…”

Section: Western Blot Analysis and Histological Immunostainingmentioning

confidence: 99%

Grim-19 expressed by recombinant adenovirus for esophageal neoplasmtarget therapy

et al. 2018

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Esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EA) are the two most common types of esophageal cancer, which is the sixth highest cause of cancer‑associated mortality and the eighth most common cancer worldwide. Gene associated with retinoid‑interferon (IFN)‑induced mortality‑19 (Grim‑19) is reported to be a cell death activator that may be used to define mechanisms involved in IFN‑β‑ and retinoic acid‑induced cell death and apoptosis in a number of tumor cell lines. The present study constructed a recombinant adenovirus expressing Grim‑19 (rAd‑Grim‑19) and investigated its therapeutic outcomes in ESCC cells and tumor‑bearing mice. Grim‑19 expression was detected in EC‑109 (ESCC) cells by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. Tumor cell death and apoptosis induced by rAd‑Grim‑19 in EC‑109 cells were analyzed by flow cytometry. The inhibitory effects of rAd‑Grim‑19 on EC‑109 growth were determined by MTT assays. Furthermore, the therapeutic effects of rAd‑Grim‑19 were investigated in EC‑109‑bearing mice. The results demonstrated that Grim‑19 mRNA and protein expression was downregulated in EC‑109 esophageal carcinoma cells compared with Het‑1A normal esophageal epithelial cells. In addition, EC‑109 cells exhibited a significant reduction in tumor cell growth in the rAd‑Grim‑19 group compared with the control groups. Furthermore, rAd‑Grim‑19 increased EC‑109 cell apoptosis compared with the control group. These results indicated that rAd-Grim-19 may regulate tumor cell growth and apoptosis. Additionally, the results demonstrated that rAd‑Grim‑19 led to beneficial outcomes and prolonged the survival of esophageal tumor‑bearing mice. In conclusion, the present study demonstrated that rAd‑Grim‑19 may have potential as an antitumor agent for esophageal neoplasms and may therefore be beneficial for patients with esophageal neoplasms.

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Do Esophageal Squamous Cell Carcinoma Patients Have an Increased Risk of Coexisting Colorectal Neoplasms?

Cited by 2 publications

References 10 publications

Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer

Targeting cysteine‑rich angiogenic inducer‑61 by antibody immunotherapy suppresses growth and migration of non‑small cell lung cancer

Grim-19 expressed by recombinant adenovirus for esophageal neoplasmtarget therapy

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