FoxM1 is Overexpressed in <i>Helicobacter pylori</i>–Induced Gastric Carcinogenesis and Is Negatively Regulated by miR-370

Feng, Yimin; Wang, Lixiang; Zeng, Jiping; Shen, Li; Liang, Xiao; Yu, Han; Liu, Shili; Liu, Zhifang; Sun, Yuan; Li, Wenjuan; Chen, Chunyan; Jia, Jihui

doi:10.1158/1541-7786.mcr-13-0007

Cited by 86 publications

(58 citation statements)

References 43 publications

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“…It is known that both CIP2A and H. pylori infection enhance cell proliferation (15,16,(37)(38)(39). In the present study, blocking of CIP2A by its specific siRNA significantly attenuated H. pylori-induced cell proliferation, suggesting that H. pylori induced the proliferation of gastric epithelial cells through upregulation of CIP2A.…”

Section: Discussionsupporting

confidence: 57%

Helicobacter pylori enhances CIP2A expression and cell proliferation via JNK2/ATF2 signaling in human gastric cancer cells

Zhao

Han

et al. 2014

International Journal of Molecular Medicine

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Abstract.Helicobacter pylori (H. pylori) infection plays an important role in the development of gastric carcinomas. Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a novel human oncoprotein that functions as an important regulator of cell growth and malignant transformation. In the present study, we aimed to investigate the potential mechanisms by which H. pylori upregulates the expression of CIP2A and the functional impact of H. pylori-induced CIP2A in gastric cancer cells. We demonstrated that infection of MKN-45 cells with H. pylori led to a marked increase in the expression of CIP2A at the mRNA and protein levels. H. pylori-induced CIP2A was associated with increased cell proliferation. In addition, H. pylori was found to activate the JNK2 pathway. Importantly, both H. pylori-induced CIP2A production and cell proliferation were partially reversed by inhibition of JNK2 signaling. Similarly, the blockade of H. pylori-induced CIP2A expression by siRNA against CIP2A also inhibited cell proliferation. Thus, H. pylori appears to stimulate the expression of CIP2A and proliferation of gastric cancer cells via JNK2 signaling. These findings suggest that H. pylori-induced upregulation of CIP2A contributes to the development and progression of gastric cancer. Further in vivo studies are warranted to explore the biological role of CIP2A and its interaction with JNK2 signaling in gastric cancer.

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Section: Discussionsupporting

confidence: 57%

Helicobacter pylori enhances CIP2A expression and cell proliferation via JNK2/ATF2 signaling in human gastric cancer cells

Zhao

Han

et al. 2014

International Journal of Molecular Medicine

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“…1a), whereas a high dose of CoCl 2 showed ototoxicity as evidenced by decreased viability. These results indicated that CoCl 2 was able to promote proliferation of HUVECs as reported [13][14][15]. After the CoCl 2 -induced hypoxic proliferation model was established, the potential toxicity of propranolol on HUVECs was evaluated.…”

Section: Effects Of Propranolol and Cocl 2 On Huvec Viabilitysupporting

confidence: 78%

Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro

Zhang

et al. 2018

Pharmacology

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Background/Aims: To investigate the effect of propranolol on cobalt chloride (CoCl₂)-induced hypoxic proliferation in human umbilical vein endothelial cells (HUVECs). Methods: CoCl₂ was administrated to HUVECs to mimic hypoxic proliferation in infantile hemangioma. The proliferation of HUVECs was detected by Cell Counting Kit-8. Effects of propranolol on apoptosis and expressions of cell cycle-related genes, CDK4 and cyclin D1, were detected by flow cytometry and RT-PCR respectively. The release of vascular endothelial growth factor (VEGF) and lactate dehydrogenase (LDH) was measured by enzyme-linked immunosorbent assay. Results: Propranolol significantly inhibited the CoCl₂-induced hypoxic proliferation of HUVECs in a dose-dependent manner, and also induced apoptosis and suppressed the expression of CDK4 and cyclin D1. Propranolol also decreased the release of VEGF and LDH in the supernatant. Conclusions: Propranolol could inhibit CoCl₂-induced hypoxic proliferation of HUVECs through inducing apoptosis and cell cycle arrest.

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“…Zhang et al reported that H.pylori infection upregulated the expression of miR-21, which in turn downregulated the expression of reversion-inducing-cysteine-rich protein with Kazalmotifs (RECK), leading to the development of gastric cancer [11]. In addition, H.pylori infection downregulated the expression of miR-370, and then, miR-370 promoted cell proliferation by regulating the expression of FoxM1 in gastric cancer cells [12]. In our previous study, using microarray analysis, we showed that miR-29a-3p was upregulated in H.pylori-infected gastric epithelial cells (GES-1).…”

Section: Introductionmentioning

confidence: 99%

microRNA-29a-3p, Up-Regulated in Human Gastric Cells and Tissues with H.Pylori Infection, Promotes the Migration of GES-1 Cells via A20-Mediated EMT Pathway

Sun

Zhu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Helicobacter pylori (H. pylori) infection is closely related to human gastric mucosa-associated diseases. Several recent studies on miRNAs have expanded our insights on H.pylori pathogenesis. This study aimed to investigate the biological roles and underlying molecular mechanisms of miR-29a-3p in human gastric cells and tissues with H.pylori infection. Methods: miR-29a-3p expression was quantified by quantitative RT-PCR (qRT-PCR). A miR-29a-3p target gene was validated by bioinformatics analysis, western blotting and dual luciferase reporter gene assays. Western blotting and immunohistochemistry (IHC) assay were performed to detect the protein expression. Transwell assay was used to determine the cell migration ability. Results: MiR-29a-3p was up-regulated in H.pylori-positive gastric mucosa tissues and H.pylori-infected gastric cells. The up-regulation of miR-29a-3p was dose-dependent in BGC-823 and GES-1 cells infected with H.pylori. Using gain- and loss-of-function experiments in vitro, we demonstrated that miR-29a-3p promoted the migration of gastric epithelial cells. We further characterized A20 as a direct target of miR-29a-3p. The expression of A20 was decreased in H.pylori-positive gastric mucosa tissues compared with H.pylori-negative gastric mucosa tissues. A20 downregulation was time- and dose-dependent in GES-1 and BGC-823 cells infected with H.pylori. In GES-1 and BGC-823 cells infected with H.pylori, the miR-29a-3p mimic significantly blocked A20 expression, which suggests that H.pylori decreased A20 expression through up-regulating miR-29a-3p in GES-1 and BGC-823 cells infected with H.pylori. The knockdown of A20 by siRNA enhanced the migration of human gastric epithelial cells and promoted the expression of Snail, Vimentin, and N-cadherin and inhibited the expression of E-cadherin. Conclusion: The miR-29a-3p may act as a tumor promotive miRNA by regulating cells migration through directly targeting of A20 gene in human gastric epithelial cells infected with H.pylori.

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FoxM1 is Overexpressed in Helicobacter pylori–Induced Gastric Carcinogenesis and Is Negatively Regulated by miR-370

Cited by 86 publications

References 43 publications

Helicobacter pylori enhances CIP2A expression and cell proliferation via JNK2/ATF2 signaling in human gastric cancer cells

Helicobacter pylori enhances CIP2A expression and cell proliferation via JNK2/ATF2 signaling in human gastric cancer cells

Propranolol Suppresses Cobalt Chloride-Induced Hypoxic Proliferation in Human Umbilical Vein Endothelial Cells in vitro

microRNA-29a-3p, Up-Regulated in Human Gastric Cells and Tissues with H.Pylori Infection, Promotes the Migration of GES-1 Cells via A20-Mediated EMT Pathway

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