Upregulation of miR-370 contributes to the progression of gastric carcinoma via suppression of FOXO1

Liu, Sheng; Zhao, Yijie; Han, Youqun; Yang, Longqiu; Tao, Guorong; Li, Qing; Zhang, Lei

doi:10.1016/j.biopha.2013.04.014

Cited by 42 publications

(25 citation statements)

References 19 publications

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“…This is consistent with the result from one previous study in which upregulation of miR-370 promoted cell apoptosis and inhibited proliferation via targeting PTEN in human GC (21). However, studies also found that upregulation of miR-370 contributed to the progression of gastric carcinoma (36,37). The explanation for this may be due to the different functions of the targeted gene.…”

Section: Discussionsupporting

confidence: 92%

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

et al. 2017

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Epidermal growth factor receptor (EGFR) is known to be overexpressed in ~30% of gastric cancer (GC) cases, and may serve as an effective biomarker for predicting the clinical benefit of anti-EGFR therapy. However, the mechanism underlying the regulation of EGFR expression remains unknown. Evidence indicates that post-transcriptional regulation may exist in the process of EGFR expression. In the present study, we aimed to explore whether miR-370 is involved in this process, and how it impacts the biological behaviors of GC cells. In the present study, we first determined the role of EGFR in GC by means of an EGFR overexpression plasmid and siRNAs. Then, the expression levels of EGFR protein and mRNA in GC tissues were analyzed through immunohistochemistry and quantitative RT-PCR (RT-qPCR). Bioinformatics tools and dual-luciferase assay were applied to predict and validate the relevant miRNA targeting EGFR. Finally, human GC MGC-803 cells were selected to explore the effect of miRNA on cell proliferation and migration. We found that suppression of EGFR inhibited the proliferation and migration of GC cells. In addition, the levels of EGFR protein in the GC tissues were ~4 times higher than that in the corresponding paired non-cancerous tissues while the mRNA levels of EGFR were only ~2-fold as high as that in the adjacent non-cancerous tissues. Bioinformatics tools predicted that miRNA-370 was a regulator of EGFR and dual‑luciferase assay validated that miR-370 could directly bind to the 3'-untranslated region (3'-UTR) of EGFR mRNA. Meanwhile, an inverse correlation between miR-370 and EGFR was found in the GC tissues. Overexpression of miR-370 suppressed the proliferation and migration of GC cells, while downregulation of miR-370 promoted proliferation and migration. The present study may provide new information for understanding the molecular mechanism underlying the regulation of EGFR protein expression in GC and may be of important clinical significance to guide targeted therapy.

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Section: Discussionsupporting

confidence: 92%

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

et al. 2017

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“…Overall, our results showed that miRNAs miR-103, miR-181c, miR-370 and miR-375 are down-regulated in chronic gastritis regardless of H. pylori infection, because both infected and non-infected sample groups had reduced expression of these miRNAs. Other studies have shown down-regulation of miRNAs in inflammatory gastric lesions infected or non-infected by H. pylori (Matsushima et al, 2011;Shiotani et al, 2012); however, in gastric cancer some studies have reported increased expression of miRNAs such as miR-103, miR-181c, miR-370, miR-21 and miR-146a (Wu et al, 2011;An et al, 2013;Fan et al, 2013;Ishimoto et al, 2016). This different expression profile between gastric cancer and H. pylori infected gastric mucosa suggests that these miRNAs might act differently in the distinct stages of gastric tumorigenesis and disease progression.…”

Section: Discussionmentioning

confidence: 99%

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

Rossi

Cadamuro

Biselli

et al. 2016

Cellular Microbiology

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Summary Helicobacter pylori cause chronic inflammation favouring gastric carcinogenesis, and its eradication may prevent malignant transformation. We evaluated whether H. pylori infection and its eradication modify the expression of inflammatory mediators in patients with chronic gastritis. Furthermore, we assessed whether microRNAs modulate inflammatory pathways induced by H. pylori and identified miRNA–gene interaction networks. mRNA and protein expression of TNFA, IL6, IL1B, IL12A, IL2 and TGFBRII and miRNAs miR‐103a‐3p, miR‐181c‐5p, miR‐370‐3p, miR‐375 and miR‐223‐3p were evaluated in tissue samples from 20 patients with chronic gastritis H. pylori negative (Hp−) and 31 H. pylori positive (Hp+), before and three months after bacterium eradication therapy, in comparison with a pool of Hp− normal gastric mucosa. Our results showed that H. pylori infection leads to up‐regulation of TNFA, IL6, IL12A and IL2 and down‐regulation of miRNAs. Bacterium eradication reduces the expression of TNFA and IL6 and up‐regulates TGFBRII and all investigated miRNAs, except miR‐223‐3p. Moreover, transcriptional profiles of inflammatory mediators and miRNAs after eradication are different from the non‐infected group. Deregulated miRNA–mRNA interaction networks were observed in the Hp+ group before and after eradication. Therefore, miRNAs modulated cytokine expression in the presence of H. pylori and after its eradication, suggesting that miRNAs participate in the pathological process triggered by H. pylori in the gastric mucosa.

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“…Furthermore, miR-320 has been described to downregulate the expression of IGF-1 and its receptor (52,54). MiR-370 has been shown to be a FOXO1 gene regulator in prostatic cancer cells (55,56). It is also described as a regulator of Insulin receptor substrate 1 (IRS1), an insulin-signaling scaffold-protein (37,38,55).…”

Section: Discussionmentioning

confidence: 99%

MiRNAs Regulating Insulin Sensitivity Are Dysregulated in Polycystic Ovary Syndrome (PCOS) Ovaries and Are Associated With Markers of Inflammation and Insulin Sensitivity

et al. 2019

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Objective: MicroRNAs (miRNAs) are gene expression regulators. Altered miRNA levels are associated with diabetes, insulin resistance, and inflammation. Insulin resistance and inflammation are both features of Polycystic ovary syndrome (PCOS). The aim of this study was first to assess differences in selected miRNAs (miR-146a, miR-155, miR-320, miR-370, miR-486), involved in insulin sensitivity regulation and inflammation, in women with or without PCOS. Second, to investigate relationships among these miRNAs, insulin, High mobility group box 1 (HMGB1), and IL-6 in follicular fluid (FF), serum 17-beta estradiol (E2), and the number of dominant follicles.Methods: Thirty PCOS and thirty-six non-PCOS women undergoing in vitro fertilization were enrolled. RNA from granulosa cells (GC) and FF was extracted and the specific miRNAs were evaluated using qRT-PCR. HMGB1, insulin, and IL-6 in FF, and serum E2 were assayed using specific kits.Results: MiR-146a, miR-155, miR-486 were upregulated and miR-320 and miR-370 were downregulated in GC from the PCOS patients. In FF, miR-146a, miR-155, and miR-486 showed lower levels in PCOS, whereas miR-320 and miR-370 showed an opposite trend but no significant changes were observed. These miRNAs showed relationships with Body Mass Index (BMI), age, E2, number of dominant follicles, insulin, and HMGB1. Conclusion:In conclusion, the miRNAs analyzed showed changes in PCOS ovaries and had relationships with indices of inflammation and insulin sensitivity within the ovary, providing evidence for new regulatory mechanisms.

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Upregulation of miR-370 contributes to the progression of gastric carcinoma via suppression of FOXO1

Cited by 42 publications

References 19 publications

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

miR-370 regulates cell proliferation and migration by targeting EGFR in gastric cancer

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection

MiRNAs Regulating Insulin Sensitivity Are Dysregulated in Polycystic Ovary Syndrome (PCOS) Ovaries and Are Associated With Markers of Inflammation and Insulin Sensitivity

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