[Retracted] MicroRNA­145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the cell apoptotic assay data shown in Figs. 3D and 4D were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive any reply. The Editor apologizes to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 13: 1033­1039, 2016; DOI: 10.3892/mmr.2015.4609].

Epigenetic silencing of miR-181b contributes to tumorigenicity in colorectal cancer by targeting RASSF1A.

Aberrant microRNA expression is common in colorectal cancer and DNA methylation is believed to be responsible for this alteration. In this study, we performed evaluation in vivo and in vitro to determine the role of miR-181b as a potential diagnostic and prognostic biomarker in colorectal cancer. Ninety-seven pairs of colorectal cancer tissues and adjacent normal tissues were collected. The expression level and methylation status of miR-181b was determined in tissue samples and multiple colorectal cancer cell lines. RASSF1A, a predicted target gene of miR-181b, was investigated in vitro. Further mechanistic explorations were conducted. It was found that miR-181b expression was frequently downregulated in cancer samples. This lower expression level resulted from higher hypermethylation in cancer tissue and was closely related to TNM stage. Following artificial synthesis of miR-181b stimulation, colorectal cancer cell proliferation was greatly inhibited in CRC cells while apoptosis percentage markedly increased. miR-181b achieved the tumor suppressive effects via direct targeting of the RASSF1A gene. This study indicated the clinical significance of miR-181b and the influence of miR-181b promoter region in epigenetic silencing of tumorigenicity in colorectal cancer, and implied the possible usage of miR-181b as a diagnostic and prognostic biomarker in colorectal cancer.

MicroRNA­145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression.

MicroRNA (miR)­145 has been demonstrated to act as a tumor suppressor, and deregulation of fascin 1 (FSCN1) has been observed in several types of human malignancy, including gastric carcinoma. However, the molecular mechanism underlying the function of miR­145, specifically its targets in gastric carcinoma have yet to be fully elucidated. In the present study, downregulation of miR­145 and upregulation of FSCN1 was identified in gastric carcinoma cell lines, compared with normal gastric mucosal epithelial cells. A luciferase reporter assay demonstrated that miR­145 was able to bind to the 3'­untranslated region of FSCN1 mRNA. Overexpression of miR­145 led to a significant decrease in FSCN1 expression levels, whereas knockdown of miR­145 resulted in increased FSCN1 expression levels in gastric carcinoma cells. Furthermore, overexpression of miR­145 inhibited proliferation, migration and invasion in gastric carcinoma cells. Similar effects were also observed in gastric carcinoma cells transfected with FSCN1 small interfering RNA. In addition, overexpression of FSCN1 reversed the suppressive effects of miR­145 upregulation on proliferation, migration and invasion in gastric carcinoma cells, suggesting that FSCN1 is indeed involved in the miR­145­mediated malignant phenotype of gastric carcinoma cells. The present study revealed an anti­oncogenic role of miR­145 in gastric carcinoma via inhibition of FSCN1, and suggested that miR­145 may be used for the treatment of gastric carcinoma.

High expression of astrocyte elevated gene-1 is associated with clinical staging, metastasis, and unfavorable prognosis in gastric carcinoma.

More and more evidence has demonstrated that astrocyte elevated gene-1 (AEG-1) is tightly associated with progression, metastasis, and unfavorable prognosis in many malignancies. However, the potential biological role of AEG-1 in gastric carcinoma (GC) has not been thoroughly delineated. In the current study, we found that AEG-1 mRNA and protein levels in GC tissues were significantly higher than those in normal gastric mucosa (P < 0.05). Simultaneously, statistical analysis displayed a significant correlation of high AEG-1 mRNA and protein expressions with differentiation status, TNM staging, invasive depth, and lymph node metastasis (P < 0.05). Most importantly, expressions of AEG-1 mRNA and protein in high clinical staging and metastatic GC tissues were dramatically higher than those in low clinical staging and non-metastatic GC tissues (P < 0.05). Stepwise investigation confirmed that the survival time of the patients with high AEG-1 level was shorter than those with low AEG-1 level or negative AEG-1 staining. Taken altogether, our data presented herein suggest that AEG-1 may be a novel predictor for metastasis and prognosis of the patients with GC.

miR-27a as an oncogenic microRNA of hepatitis B virus- related hepatocellular carcinoma.

microRNAs (miRNAs) are small non-coding RNAs that regulate gene expression through post-transcriptional interactions with mRNA. miRNAs have recently emerged as key regulators of various cancers. Although miR- 27a has been implicated in several other cancers, its role in hepatitis B virus-related hepatocellular carcinoma (HCC) is unknown. In this study, we showed miR-27a to be frequently up-regulated in HCC tissues and HCC cell lines (HepG2 and Huh7). Overexpression of miR-27a enhanced cell proliferation, promoted migration and invasion, and activated cell cycling in HepG2 and Huh7 cells. In summary, our results suggest that up-regulation of miR-27a may play an oncogenic role in the development of HCC and might thus be a new therapeutic target in HCC patients.