miR-204 targets Bcl-2 expression and enhances responsiveness of gastric cancer

Sacconi, Andrea; Biagioni, Francesca; Canu, Valeria; Mori, Federica; Benedetto, Anna Di; Lorenzon, Laura; Ercolani, Cristiana; Agostino, Silvia Di; Cambria, A; Germoni, Sabrina; Grasso, Giuseppe; Blandino, R.; Panebianco, Vincenzo; Ziparo, Vincenzo; Federici, Orietta; Muti, Paola; Strano, Sabrina; Carboni, Fabio; Mottolese, Marcella; Diodoro, Maria Grazia; Pescarmona, Edoardo; Garofalo, Alfredo; Blandino, Giovanni

doi:10.1038/cddis.2012.160

Cited by 161 publications

(157 citation statements)

References 27 publications

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“…47,48 Recent studies showed that SIRT1 is a target for miR-204 and is functionally critical for multiple cancer phenotypes such as migration/invasion, EMT, and resistance to anoikis. 17,49,50 Consistent with these studies, we showed that both MALAT1 and SIRT1 bound to the same site on miR-204, and therefore, in addition to targeting miR-204 to Ago2-mediated silencing, MALAT1 may also compete with SIRT1 for binding to miR-204, both mechanisms releasing SIRT1 from the negative control by miR-204.…”

Section: Discussionmentioning

confidence: 99%

The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Hou

Zhou

et al. 2017

Tumour Biol.

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Increasing evidence supports the significance of long non-coding RNA in cancer development. Several recent studies suggest the oncogenic activity of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in hepatocellular carcinoma. In this study, we explored the molecular mechanisms by which MALAT1 modulates hepatocellular carcinoma biological behaviors. We found that microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis. Through bioinformatic screening, luciferase reporter assay, RNA-binding protein immunoprecipitation, and RNA pull-down assay, we identified microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells. Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.

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Section: Discussionmentioning

confidence: 99%

The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Hou

Zhou

et al. 2017

Tumour Biol.

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“…As Ezrin is critical to Ras activation and is predicted to be a target of miR-204, this indicates that miR-204 downregulation may be a novel mechanism for aberrant Ras activation in gastric tumorigenesis (Lam et al, 2011). Further, miR-204 may target Bcl-2 expression and increase the responsiveness of GC cells to 5-fluorouracil and oxaliplatin treatment, indicating that miR-204 might be a therapeutic target for improving the prognosis of GC (Sacconi et al, 2012). Wang et al (2014) compared differentially expressed miRNAs between Helicobacter pylori-related gastritis and gastric intestinal metaplasia lesions.…”

Section: Discussionmentioning

confidence: 99%

Reduced expression of serum miR-204 predicts poor prognosis of gastric cancer

Chen

Liu

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Deregulation of microRNAs (miRNAs) is implicated in the initiation and progression of gastric cancer (GC). Previous studies have demonstrated that miR-204 was downregulated in GC tissues. However, its expression profile in serum samples and its potential for clinical value remain unknown. Real-time PCR was performed to evaluate the expression level of serum miR-204 in patients with GC. The association between serum miR-204 expression level and the clinical outcome of GC was then investigated. Our results showed that the expression of miR-204 in serum samples from GC patients was significantly lower than that in the healthy controls (P < 0.01). Serum miR-204 expression level of GC patients was significantly upregulated after receiving surgical resection (P < 0.01). In addition, serum miR-204 was associated with lymph node metastasis (P = 0.016), tumor differentiation (P = 0.001), and TNM stage (P = 0.005). GC patients with low serum miR-204 expression had shorter overall survival than those with high serum miR-204 expression (P = 0.004). Multivariate analysis revealed that serum miR-204 expression level was an independent risk factor for this malignant disease (HR = 3.629, 95%CI = 2.828-8.146, P = 0.015). In conclusion, our findings indicate that serum miR-204 may be employed as a novel biomarker for monitoring the treatment response and predicting the prognosis of GC.

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“…In addition, downregulation of miR-204 has been documented in several types of cancers. [37][38][39][40][41] Decreased expression of miR-204 results in overexpression of its target, myeloid cell leukemia sequence 1 (Mcl-1) mRNA, and induces anti-apoptotic signaling in pancreatic cancers. 42 miR-204 also regulates expression of an oncogene, neurotrophic receptor tyrosine kinase B, and promotes metastasis in endometrial carcinoma.…”

Section: Discussionmentioning

confidence: 99%