[Corrigendum] MicroRNA-148a inhibits breast cancer migration and invasion by directly targeting WNT-1.

Subsequently to the publication of the above article, an interested reader drew to the authors' attention that the data panel for the MDA­MB­231/migration/NC experiment in Fig. 2B on p. 1428 was strikingly similar to the data shown for the MDA­MB­231/invasion/Blank experiment in Fig. 2C, such that these data appeared to have been derived from the same original source. The authors have referred back to their original data, and realize that the data panel was selected incorrectly for Fig. 2B. The corrected version of Fig. 2, showing the correct data for the MDA­MB­231/migration/NC experiment in Fig. 2B, is shown on the next page. The authors regret the error that was made during the preparation of this figure, and can confirm that the error in the assembly of this figure did not adversely affect the conclusions reported in the study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 35: 1425­1432, 2016; DOI: 10.3892/or.2015.4502].

Upregulated expression of ACTL8 contributes to invasion and metastasis and indicates poor prognosis in colorectal cancer.

BACKGROUND: ACTL8 is a member of the CT antigens. There are only few studies on the role of ACTL8 in malignant tumors. The aim of this study is to investigate the expression and clinical significance of ACTL8 protein in colorectal cancer (CRC). MATERIALS AND METHODS: Human CRC tissues and cell lines, and paired adjacent non-tumor tissues and human intestinal epithelial cell lines were obtained to evaluate the expression of ACTL8. The association between protein expression of ACTL8 and clinicopathological parameters and prognosis of CRC patients was examined. The biological functions of ACTL8 in the invasion and metastasis of CRC were determined by wound healing and transwell invasion assays after silencing of ACTL8 in CRC cell lines. The potential target genes of ACTL8 were also identified by quantitative reverse transcription PCR and Western blotting after silencing of ACTL8 in CRC cell lines. RESULTS: It was found that ACTL8 was upregulated in human CRC tissues and cell lines. The expression of ACTL8 was positively associated with poor differentiation, invasion and metastasis, postoperative infection, and poor prognosis, but negatively associated with proximal margin length. In addition, silencing of ACTL8 significantly decreased the capacity of invasion and migration in HT29 and SW620 CRC cell lines. Moreover, silencing of ACTL8 significantly decreased the expression of TRIM29 in HT29 and SW620 CRC cell lines. CONCLUSION: These results suggest that ACTL8 plays a key role in the invasion and metastasis of CRC, and TRIM29 may be involved in the ACTL8-mediated poor prognosis of CRC.

Morin enhances hepatic Nrf2 expression in a liver fibrosis rat model.

AIM: To investigate whether morin can reduce hepatic fibrosis by activating the NF-E2-related factor 2 (Nrf2) signaling pathway. METHODS: Twenty male Sprague-Dawley rats were randomly divided into four groups: control group, morin group, carbon tetrachloride (CCl4) group, and morin + CCl4 group. Rats in both the CCl4 and morin + CCl4 groups were injected intraperitoneally with CCl4 at a dose of 2 mL/kg twice a week. Rats in both the morin and morin + CCl4 groups were treated orally with morin at a dose of 50 mg/kg twice a week. Control rats were treated with vehicle only twice a week. At the end-point of the 8 wk of the experimental period, serum AST, ALT, and ALP were measured, and the liver specimens were obtained for pathological assessment. Real-time PCR and Western blot methods were used to analyze the expression of α-smooth muscle actin (α-SMA), collagen I, collagen III, Nrf2, heme oxygenase (HO-1), and quinone oxidoreductase 1 (NQO1) using frozen liver specimens. RESULTS: Morin-treated rats in the morin + CCl4 group had less hyperplasia of fiber tissue, minimal inflammatory cells, and less body weight loss with favorable liver enzyme measurements compared to rats treated with CCl4 only. Additionally, morin-treated rats had significantly lower mRNA and protein expression of α-SMA, collagen I, and collagen III, but significantly higher mRNA and protein expression of Nrf2, HO-1, and NQO1 compared to rats treated with CCl4 only (P < 0.05). CONCLUSION: Morin could play a protective role by inducing the expression of Nrf2 and its downstream antioxidant factors (HO-1 and NQO1) and reducing the expression of α-SMA, collagen I, and collagen III in CCl4-induced liver fibrosis rats.

MicroRNA-148a inhibits breast cancer migration and invasion by directly targeting WNT-1.

Wnt/ß-catenin signaling pathway influences embryonic development, cell polarity and adhesion, apoptosis and tumorigenesis. MicroRNAs (miRNAs) function as important regulators of the tumorigenesis and metastasis. In the present study, we aimed to find novel targets and mechanisms of microRNA-148a (miR-148a) in regulating the migration and invasion of breast cancer cells. In the present study, miR-148a was found downregulated in human breast cancer tissues and cell lines. The ectopic miR-148a expression inhibited the migration and invasion of MCF-7 and MDA-MB-231 breast cancer cells. Furthermore, we demonstrated that WNT-1, one of the ligands of Wnt/ß-catenin signaling pathway, was a direct target of miR-148a. The overexpression of miR-148a reduced the mRNA and protein expression levels of WNT-1, also decreased the expression levels of the key components of Wnt/ß-catenin pathway, including ß-catenin, metalloproteinase-7 (MMP-7) and T-cell factor-4 (TCF-4) in MCF-7 and MDA-MB-231 cells. In addition, the data showed that the expression of WNT-1 was significantly higher in human breast cancer tissues compared with the adjacent normal tissues and the expression of miR-148a was negatively correlated with the WNT-1 expression in human breast cancer tissues. Taken together, our results suggest that miR-148a can suppress the migration and invasion of breast cancer cells by targeting WNT-1 and inhibiting Wnt/ß-catenin signaling pathway and this will provide new insights into the molecular mechanisms of breast cancer metastasis.