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Huixia Wang,1 Ruzhen Jia,1 Tianle Lv,1 Mei Wang,1 Shiwei He,1 Xia Zhang2 1Respiratory Department, The People’s Hospital of Baoji City, Baoji, Shaanxi 721000, People’s Republic of China; 2Department of Pulmonary and Critical Care Medicine, Central Hospital of Hanzhong City, Hanzhong, Shaanxi 723000, People’s Republic of ChinaCorrespondence: Xia ZhangDepartment of Pulmonary and Critical Care Medicine, Central Hospital of Hanzhong City, No. 277, Kangfu Road, Hanzhong, Shaanxi 723000, People’s Republic of ChinaTel/ Fax +86 916-2680145Email zhangxia01056@163.comBackground: The STAT3/HIF-1α/VEGF pathway is associated with the development and progress of various tumors including NSCLC. The aim of the present study was to investigate whether resveratrol (RES) could suppress NSCLC progression via inhibiting the expressions of STAT3, HIF-1α, and VEGF in a nude rat model.Methods: Twenty-four nude rats were randomly divided into control, NSCLC, and NSCLC+RES groups. An orthotopic rat model of NSCLC was established. The animals in the NSCLC+RES group received the same operation as the NSCLC group and were intragastrically administered RES at 250 mg/kg/day for 12 weeks. Lung tissue samples were harvested for gross tumor burden measurement, histological examinations, RT-PCR, and Western blot assays.Results: In the NSCLC+RES group, significant decreases in lung weight index, lung tumor burden, STAT3/HIF-1α/VEGF mRNA, and protein levels were observed when compared with the NSCLC group (all P< 0.05). The structural integrity of the lung was less affected and the apoptotic index was significantly higher in the NSCLC+RES group, when compared to the NSCLC group (P< 0.05).Conclusion: RES suppresses NSCLC partly through inhibiting the expressions of STAT3, HIF-1α, and VEGF. The STAT3/HIF-1α/VEGF pathway might be a candidate drug target for developing new chemotherapy agents derived from RES for the treatment of NSCLC.Keywords: resveratrol, non-small-cell lung cancer, STAT3, HIF-1α, VEGF, rat

Changqin Xu, Bin Li, Shulei Zhao, Bingjie Jin, Ruzhen Jia, Jian Ge, Hongwei Xu Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, People’s Republic of ChinaCorrespondence: Hongwei XuDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong University, 324 Jingwu Road, Huaiyin District, Jinan, Shandong 250021, People’s Republic of China250021 Email jiesu10737309@163.comObjective: MicroRNA (miRNA) is an endogenous, non-coding small RNA that plays a key role in regulating organism biology and pathology. The aim of this study was to investigate the expression characteristics of microRNA-186-5p in esophageal cancer (ECa) and its correlation with clinical progression and prognosis, and to further explore its underlying mechanisms.Methods: Real-time quantitative PCR (qRT-PCR) was used to detect microRNA-186-5p level in 45 pairs of ECa tissue samples and adjacent ones, and to analyze the expression of microRNA-186-5p and clinical progression of ECa and prognosis. The relationship between microRNA-186-5p level in ECa cell lines was further verified by qRT-PCR. Finally, the potential mechanism was explored using luciferase reporter gene assay and cell recovery experiment.Results: QRT-PCR results revealed that the expression of microRNA-186-5p in ECa tissues was remarkably lower than that in adjacent tissues, and the difference was statistically significant. Compared with patients with high expression of microRNA-186-5p, patients with low expression of microRNA-186-5p had higher incidence of pathological stage and lower overall survival rate. Besides, compared with the miR-NC group, the microRNA-186-5p mimics group had a significant decrease in proliferation and metastasis ability of ECa cells. Subsequent qRT-PCR validation in ECa cell lines and tissues indicated a significant increase in HOXA9 expression and a negative correlation with microRNA-186-5p.Conclusion: The expression of microRNA-186-5p was remarkably decreased in ECa, which was remarkably correlated with pathological stage, distant metastasis and poor prognosis of ECa. The results suggested that microRNA-186-5p may inhibit cell proliferation of ECa by regulating HOXA9.Keywords: microRNA-186-5p, HOXA9, esophageal cancer, proliferation, metastasis