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3 results on '"Wei-Qiang Hong"'

1. MiR-499-5p protects cardiomyocytes against ischaemic injury via anti-apoptosis by targeting PDCD4

Author

Xue-Ming Bao, Wei-Qiang Hong, Xi-Fu Wang, Ying-Qing Li, Jian-Hua Lu, Jun-Hua Wu, and Xiongbin Li

Subjects
0301 basic medicine, Male, Programmed cell death, Pathology, medicine.medical_specialty, Primary Cell Culture, Myocardial Infarction, acute myocardial infarction, ischaemic injury, Apoptosis, miR-499-5p, Rats, Sprague-Dawley, 03 medical and health sciences, microRNA, Pathology Section, In Situ Nick-End Labeling, Medicine, Animals, Myocytes, Cardiac, cardiovascular diseases, RNA, Messenger, Cells, Cultured, Gene knockdown, business.industry, Myocardium, Hypoxia (medical), Coronary Vessels, In vitro, Research Paper: Pathology, Cell Hypoxia, Rats, Disease Models, Animal, MicroRNAs, 030104 developmental biology, Oncology, Cell culture, Gene Knockdown Techniques, Cancer research, medicine.symptom, Signal transduction, programmed cell death 4, business, Apoptosis Regulatory Proteins, cardiomyocytes apoptosis, Signal Transduction
Abstract

Recent studies have reported that miRNAs might play critical roles in acute myocardial infarction (AMI). The objective of this study is to investigate the role of miR-499-5p in AMI and its potential molecular mechanisms. The expression level of MiR-499-5p was remarkably decreased in the infarcted myocardial tissues and in the cultured neonatal rat cardiomyocytes induced by hypoxia. Overexpression or knockdown of miR-499-5p decreased or increased the apoptotic rates of cultured cardiomyocytes in vitro. In addition, ectopic overexpression of miR-499-5p in the rat AMI models with agomir reduced the myocardial infarct size through decreasing the cardiomyocytes apoptosis in the infarcted area of the rat hearts. PDCD4 (programmed cell death 4) was verified as a direct target of miR-499-5p by luciferase report assay, and ectopic overexpression or inhibition of miR-499-5p could inhibit or increase the PDCD4 expression at both the mRNA and protein levels. Furthermore, we found that ectopic overexpression of PDCD4 without miR-499-5p binding sites reversed miR-499-5p-mediated cardiomyocytes apoptosis. Together, these findings revealed the role of miR-499-5p in protecting the cardiomyocytes against apoptosis induced by AMI via its direct target PDCD4, which providing evidence for the miR-499-5p/PDCD4 pathway as a potential therapeutic target for patients with AMI.

Published
2016

2. MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1

Author

Xi-Fu Wang, Jian-Hua Lu, Wei-Qiang Hong, Jun-Hua Wu, Ying-Qing Li, and Xue-Ming Bao

Subjects
Male, Cancer Research, Pathology, medicine.medical_specialty, Nasopharyngeal neoplasm, miR-24, Down-Regulation, medicine.disease_cause, Metastasis, Cell growth, Mice, Invasion, Cell Movement, Cell Line, Tumor, microRNA, medicine, Nasopharyngeal carcinoma, Gene silencing, Animals, Humans, Genes, Tumor Suppressor, RNA, Messenger, Neoplasm Metastasis, Fascin homologue 1, Fascin, Cell Proliferation, Binding Sites, biology, Base Sequence, Research, Carcinoma, Microfilament Proteins, Nasopharyngeal Neoplasms, medicine.disease, Tumor Burden, Gene Expression Regulation, Neoplastic, Disease Models, Animal, MicroRNAs, Oncology, biology.protein, Cancer research, Heterografts, Ectopic expression, RNA Interference, Carcinogenesis, Carrier Proteins
Abstract

Background Increasing evidence indicates that the dysregulation of miRNAs expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. However, no study investigates the function and mechanisms of miR-24 in nasopharyngeal carcinoma (NPC). Methods Quantitative RT-PCR, MTT, colony formation, soft-agar, wound healing, Transwell migration and invasion assays, and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of miR-24 in NPC. Luciferase reporter assay, quantitative RT-PCR, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-24. Results The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P

Published
2015

3. MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1.

Author

Ying-Qing Li, Jian-Hua Lu, Xue-Ming Bao, Xi-Fu Wang, Jun-Hua Wu, and Wei-Qiang Hong

Subjects
MICRORNA, NEOPLASTIC cell transformation, LUCIFERASES, CANCER invasiveness, METASTASIS
Abstract

Background: Increasing evidence indicates that the dysregulation of miRNAs expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. However, no study investigates the function and mechanisms of miR-24 in nasopharyngeal carcinoma (NPC). Methods: Quantitative RT-PCR, MTT, colony formation, soft-agar, wound healing, Transwell migration and invasion assays, and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of miR-24 in NPC. Luciferase reporter assay, quantitative RT-PCR, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-24. Results: The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05). Ectopic expression of miR-24 inhibited the cell viability, proliferation, migration, and invasion in vitro (all P < 0.05), and suppressed the xenograft tumor growth and lung metastasis formation in vivo (all P < 0.05). Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05). Conclusions: Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target. [ABSTRACT FROM AUTHOR]

Published
2015
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