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Your search keyword '"miR-222"' showing total 4 results
Start Over Descriptor "miR-222" Journal febs letters
4 results on '"miR-222"'

1. MicroRNA-222 promotes tumorigenesis via targeting DKK2 and activating the Wnt/β-catenin signaling pathway.

Author

Li, Qifeng, Shen, Ke, Zhao, Yang, He, Xiaoguang, Ma, Chenkai, Wang, Lin, Wang, Baocheng, Liu, Jianwen, and Ma, Jie

Subjects
*MICRORNA, *CATENINS, *WNT proteins, *CELLULAR signal transduction, *SMALL interfering RNA, *CARCINOGENESIS, *GENE expression
Abstract

Highlights: [•] DKK2 was identified as a direct target of miR-222. [•] MiR-222 siRNA significantly inhibits tumorigenesis in vivo. [•] MiR-222 overexpression promotes tumorigenesis via targeting DKK2. [•] Mir-222 regulates β-catenin and the downstream genes of Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

Published
2013
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2. Increased miR-222 in H. pylori-associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK

Author

Li, Na, Tang, Bin, Zhu, En-Dong, Li, Bo-sheng, Zhuang, Yuan, Yu, Shu, Lu, Dong-shui, Zou, Quan-Ming, Xiao, Bin, and Mao, Xu-Hu

Subjects
*STOMACH cancer, *HELICOBACTER pylori infections, *DISEASE progression, *CANCER cell proliferation, *MICRORNA, *CARCINOGENESIS, *GENE expression, *MESSENGER RNA
Abstract

Abstract: Little is known about the potential role of microRNAs (miRNAs) in the carcinogenesis of gastric cancer induced by Helicobacter pylori (H. pylori). Here, we showed that microRNA-222 (miR-222) was up-regulated in H. pylori-infected gastric mucosa and gastric cancer. Ectopic expression of miR-222 promoted cell proliferation and colony formation in vitro. Mechanistically, we identified RECK as a novel target of miR-222, and also confirmed their relationship by the inverse correlation of mRNA expression ex vivo. Furthermore, we found that RNA interference silencing of RECK can mimic the oncogenic effects of miR-222. Collectively, H. pylori may function as an initiator in the process of carcinogenesis by up-regulating miR-222, which further participates in the progression of cancer by promoting proliferation and inhibiting RECK. [Copyright &y& Elsevier]

Published
2012
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3. MicroRNA-222 promotes tumorigenesis via targeting DKK2 and activating the Wnt/β-catenin signaling pathway

Author

Jianwen Liu, Qifeng Li, Baocheng Wang, Ke Shen, Lin Wang, Jie Ma, Xiaoguang He, Yang Zhao, and Chenkai Ma

Subjects
Wnt/β-catenin signaling pathway, Cell Survival, Biophysics, Apoptosis, Biochemistry, Mice, Structural Biology, RNA interference, Cell Line, Tumor, microRNA, Genetics, Gene silencing, Animals, Humans, Gene Silencing, RNA, Small Interfering, Molecular Biology, beta Catenin, Cell Proliferation, Regulation of gene expression, Base Sequence, Chemistry, DKK2, Wnt signaling pathway, LRP6, LRP5, Cell Biology, Glioma, miR-222, Cell biology, Gene Expression Regulation, Neoplastic, Wnt Proteins, MicroRNAs, Disease Progression, Intercellular Signaling Peptides and Proteins, Signal transduction, Signal Transduction
Abstract

MiR-222 in glioma can regulate cell cycle progression and apoptosis. However, the relationship between miR-222 and Wnt/β-catenin signaling pathway in glioma remains unknown. Here, we found that the Dickkopf-2 gene (DKK2) was a direct target of miR-222 by target prediction analysis and dual luciferase reporter assay. RNA interference silencing of DKK2 proved that miR-222 overexpression led to constitutive activation of β-catenin through inhibition of DKK2 expression in glioma cells. Furthermore, miR-222 siRNA significantly inhibited tumorigenesis in vivo. Finally, Western blot analysis showed that miR-222 could regulate the expression of β-catenin and the downstream genes of Wnt/β-catenin signaling pathway. Taken together, our findings reveal a new regulatory mechanism of miR-222 and suggest that miR-222 might be a potential target in glioma therapy.

Published
2013

4. Increased miR-222 in H. pylori-associated gastric cancer correlated with tumor progression by promoting cancer cell proliferation and targeting RECK

Author

Xuhu Mao, Dongshui Lu, Bosheng Li, Bin Tang, Shu Yu, Bin Xiao, En-Dong Zhu, Na Li, Quanming Zou, and Yuan Zhuang

Subjects
Small interfering RNA, Proliferation, Biophysics, medicine.disease_cause, GPI-Linked Proteins, Biochemistry, Helicobacter Infections, Structural Biology, Stomach Neoplasms, Cell Line, Tumor, microRNA, Genetics, medicine, Gastric mucosa, Gene silencing, Humans, RECK, Molecular Biology, Cell Proliferation, biology, Helicobacter pylori, Cancer, Cell Biology, miR-222, biology.organism_classification, medicine.disease, Molecular biology, MicroRNAs, medicine.anatomical_structure, Cell Transformation, Neoplastic, Tumor progression, Gastric Mucosa, Disease Progression, RNA Interference, Gastric cancer, Carcinogenesis
Abstract

Little is known about the potential role of microRNAs (miRNAs) in the carcinogenesis of gastric cancer induced by Helicobacter pylori (H. pylori). Here, we showed that microRNA-222 (miR-222) was up-regulated in H. pylori-infected gastric mucosa and gastric cancer. Ectopic expression of miR-222 promoted cell proliferation and colony formation in vitro. Mechanistically, we identified RECK as a novel target of miR-222, and also confirmed their relationship by the inverse correlation of mRNA expression ex vivo. Furthermore, we found that RNA interference silencing of RECK can mimic the oncogenic effects of miR-222. Collectively, H. pylori may function as an initiator in the process of carcinogenesis by up-regulating miR-222, which further participates in the progression of cancer by promoting proliferation and inhibiting RECK.

Published
2011

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