Search

Your search keyword '"microRNA-224-5p"' showing total 4 results
Start Over Descriptor "microRNA-224-5p" Topic cell proliferation
4 results on '"microRNA-224-5p"'

1. Anti-asthmatic miR-224-5p inhibits the FHL1/MAPK pathway to repress airway smooth muscle cell proliferation in a murine model of asthma-like airway inflammation.

Author

Zhuang, Zhifang, Zhou, Yanjuan, Xu, Jiao, and Pan, Leying

Subjects
*MUSCLE cells, *SMOOTH muscle, *CELL proliferation, *OVALBUMINS, *METHACHOLINE chloride, *INFLAMMATION, *MITOGEN-activated protein kinases
Abstract

Background: The proliferation of airway smooth muscle cells (ASMCs) contributes to the contractility and inflammation in the pathophysiology of asthma. This intrigued us to clarify the effect of microRNA (miR)-224-5p on biological characteristics of ASMCs in mice with asthma-like airway inflammation and responses through the FHL1-dependent MAPK pathway. Methods: An ovalbumin (OVA)-induced asthma mouse model was established, where ASMCs were isolated. The expression of FHL1 was determined in asthmatic mice. Artificial modulation of FHL1 expression was performed to explore its effect on airway inflammation of asthmatic mice and ASMC proliferation and apoptosis. Afterwards, we analyzed the interaction among miR-224-5p, FHL1 and the MAPK pathway, and explored their combined impacts on airway inflammation of asthmatic mice and ASMC proliferation and apoptosis. Results: FHL1 was highly expressed and miR-224-5p was poorly expressed in asthmatic mice. FHL1 was verified to be a target of miR-224-5p. Loss of FHL1 function reduced airway inflammation in asthmatic mice and proliferation of ASMCs while inducing their apoptosis. Besides, miR-224-5p inhibited the MAPK pathway by binding to FHL1. Overexpression of miR-224-5p relieved airway inflammation, inhibited ASMC proliferation, and increased apoptosis, which could be reversed by overexpression of FHL1. Conclusion: Altogether, miR-224-5p inhibited airway inflammation in asthmatic mice and ASMC proliferation through blocking the MAPK pathway by down-regulating FHL1. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

2. Long non-coding RNA ferritin heavy polypeptide 1 pseudogene 3 controls glioma cell proliferation and apoptosis via regulation of the microRNA-224-5p/tumor protein D52 axis.

Author

Zhang, Yongqiang, Li, Ying, Wang, Jing, and Lei, Ping

Subjects
*NON-coding RNA, *FERRITIN, *POLYPEPTIDES, *GLIOMAS, *CANCER genetics, *CANCER cells, *CELL proliferation, *APOPTOSIS
Abstract

The aim of the present study was to investigate the potential role and regulatory mechanism of long non-coding RNA ferritin heavy polypeptide 1 pseudogene 3 (FTH1P3) in glioma development. The expression of FTH1P3 in low- and high-grade glioma tissues was investigated using reverse transcription-quantitative polymerase chain reaction. FTH1P3 expression was overexpressed or suppressed in U251 glioma cells to examine the involvement of FTH1P3 in glioma cell proliferation and apoptosis using MTT assay and flow cytometry respectively. In addition, the regulatory association between FTH1P3, microRNA (miR)-224-5p and tumor protein (TP) D52 was investigated to elucidate the potential underlying mechanisms of FTH1P3 in glioma by luciferase reporter assay. The results revealed that FTH1P3 was up-regulated in glioma tissues, and FTH1P3 expression in high-grade glioma tissues was significantly higher compared with that in low-grade glioma tissues. Upregulation of FTH1P3 promoted glioma cell proliferation and inhibited apoptosis. Furthermore, FTH1P3 inhibited miR-224-5p expression, which in turn negatively regulated TPD52 expression. Overexpression of miR-224-5p significantly inhibited U251 cell proliferation and induced cellular apoptosis; this effect was clearly reversed following co-transfection of miR-224-5p and TPD52. These data revealed that upregulation of FTH1P3 may have promoted glioma cell proliferation and inhibited apoptosis. Thus, the miR-224-5p/TPD52 axis may be a downstream mechanism of FTH1P3 in glioma progression. The findings of the present study may provide a theoretical basis for the study of the treatment of glioma in the future. [ABSTRACT FROM AUTHOR]

Published
2018
Full Text
View/download PDF

3. miR‑224‑5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting

Author

Lele Song, Xiaobo Peng, Mingzhen Ying, Yanjun Wu, Chengtao Guo, Lixing Zhan, Xianbao Zhan, and Renxu Chang

Subjects
0301 basic medicine, Male, Cancer Research, PTEN, microRNA-224-5p, proliferation, Apoptosis, medicine.disease_cause, Cystadenocarcinoma, Mucinous, Biochemistry, 03 medical and health sciences, Mice, 0302 clinical medicine, Cell Movement, Cell Line, Tumor, microRNA, Genetics, medicine, Animals, Humans, Neoplasm Invasiveness, Molecular Biology, Aged, Cell Proliferation, Regulation of gene expression, Gene knockdown, biology, Oncogene, PTEN Phosphohydrolase, Articles, Cell cycle, Middle Aged, invasion, Gene Expression Regulation, Neoplastic, Pancreatic Neoplasms, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, pancreatic mucinous cystadenocarcinoma, Oncology, 030220 oncology & carcinogenesis, biology.protein, Cancer research, Molecular Medicine, Heterografts, Female, Pancreas, Carcinogenesis
Abstract

Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)‑224‑5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription‑quantitative PCR was used to explorethe expression of miR‑224‑5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR‑224‑5p was assessed and verified by luciferase assay. miR‑224‑5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR‑224‑5p promoted the proliferation, migration and invasion of MCC and knockdown of miR‑224‑5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR‑224‑5p. The negative correlation between miR‑224‑5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR‑224‑5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR‑224‑5p was highly expressed and served an oncogenic role in MCC. miR‑224‑5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.

Published
2020

4. Long non‑coding RNA ferritin heavy polypeptide 1 pseudogene�3 controls glioma cell proliferation and apoptosis via regulation of the microRNA‑224‑5p/tumor protein D52 axis

Author

Jing Wang, Ying Li, Yongqiang Zhang, and Ping Lei

Subjects
Adult, Male, 0301 basic medicine, Cancer Research, microRNA-224-5p, Cell, Apoptosis, Biochemistry, long non-coding RNA ferritin heavy polypeptide 1 pseudogene 3, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Genes, Reporter, Cell Line, Tumor, Glioma, microRNA, Genetics, medicine, Humans, Molecular Biology, Cell Proliferation, Regulation of gene expression, Cell growth, Chemistry, tumor protein D52, Articles, Cell cycle, Flow Cytometry, medicine.disease, Neoplasm Proteins, Gene Expression Regulation, Neoplastic, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Oncology, 030220 oncology & carcinogenesis, Cancer research, Molecular Medicine, Female, RNA Interference, RNA, Long Noncoding, Biomarkers
Abstract

The aim of the present study was to investigate the potential role and regulatory mechanism of long non‑coding RNA ferritin heavy polypeptide 1 pseudogene 3 (FTH1P3) in glioma development. The expression of FTH1P3 in low‑ and high‑grade glioma tissues was investigated using reverse transcription‑quantitative polymerase chain reaction. FTH1P3 expression was overexpressed or suppressed in U251 glioma cells to examine the involvement of FTH1P3 in glioma cell proliferation and apoptosis using MTT assay and flow cytometry respectively. In addition, the regulatory association between FTH1P3, microRNA (miR)‑224‑5p and tumor protein (TP) D52 was investigated to elucidate the potential underlying mechanisms of FTH1P3 in glioma by luciferase reporter assay. The results revealed that FTH1P3 was up‑regulated in glioma tissues, and FTH1P3 expression in high‑grade glioma tissues was significantly higher compared with that in low‑grade glioma tissues. Upregulation of FTH1P3 promoted glioma cell proliferation and inhibited apoptosis. Furthermore, FTH1P3 inhibited miR‑224‑5p expression, which in turn negatively regulated TPD52 expression. Overexpression of miR‑224‑5p significantly inhibited U251 cell proliferation and induced cellular apoptosis; this effect was clearly reversed following co‑transfection of miR‑224‑5p and TPD52. These data revealed that upregulation of FTH1P3 may have promoted glioma cell proliferation and inhibited apoptosis. Thus, the miR‑224‑5p/TPD52 axis may be a downstream mechanism of FTH1P3 in glioma progression. The findings of the present study may provide a theoretical basis for the study of the treatment of glioma in the future.

Published
2018
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results