[Corrigendum] miR­647 and miR­1914 promote cancer progression equivalently by downregulating nuclear factor IX in colorectal cancer.

Subsequently to the publication of this paper, an interested reader drew to the authors' attention that, in the scratch­wound assays shown in Fig. 3A on p. 8195, the data shown for the '0 h/NC' and '0 h/miR­1914 antagomir' data panels appeared to be strikingly similar, such that they may have been derived from the same original source. The authors have consulted their original data, and realize that the '0 h/miR­1914 antagomir' data panel was inadvertently selected incorrectly for Fig. 3A. The corrected version of Fig. 3, now showing the correct data for the '0 h/miR­1914 antagomir' data panel in Fig. 3A, is shown on the next page. Note that the errors in Fig. 3 did not significantly affect the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 16, 8189­8199, 2017; DOI: 10.3892/mmr.2017.7675].

MicroRNA-25-3p regulates osteoclasts through nuclear factor I X.

Osteoporosis is a bone metabolic disease, characterized by loss of bone density leading to fractures. Its incidence increases with age and affects patient quality of life. Although osteoclasts play a significant role in osteoporosis, their underlying regulatory mechanisms remain unclear. In this study, we found that microRNA (miR)-25-3p negatively regulates osteoclast function through nuclear factor I X (NFIX). Overexpression of NFIX promoted osteoclast proliferation and increased the expression of the osteoclast differentiation and activity markers tartrate-resistant acid phosphatase and cathepsin K. MiR-25-3p transfection inhibited NFIX expression, which in turn inhibited osteoclast proliferation. Collectively, our results suggest that miR-25-3p promotes osteoclast activity by regulating the expression of NFIX. Therefore, targeting miR-25-3p in osteoclasts could be a promising strategy for treating skeletal disorders involving reduced bone formation.

Prognostic value of combined and individual expression of microRNA-1290 and its target gene nuclear factor I/X in human esophageal squamous cell carcinoma.

BACKGROUND: microRNA (miR)-1290 was previously indicated to promote esophageal squamous cell carcinoma (ESCC) progression via regulating its target gene nuclear factor I/X (NFIX). OBJECTIVE: To investigate clinical significance of miR-1290 and NFIX in ESCC. METHODS: Quantitative real-time PCR was performed to detect miR-1290 and NFIX mRNA expression in ESCC tissues. Associations of miR-1290 and/or NFIX mRNA expression with various clinicopathological features and prognosis in ESCC patients were statistically evaluated. RESULTS: Compared to noncancerous esophageal mucosa, miR-1290 expression was upregulated, while NFIX mRNA expression was downregulated in ESCC tissues. There was a significantly negative correlation between miR-1290 and NFIX expression in ESCC tissues (r=-0.427, P= 0.01). Interestingly, miR-1290-high and/or NFIX-low expression were all significantly associated with positive lymph node metastasis and advanced tumor-node-metastasis stage of ESCC patients (all P< 0.05). Moreover, miR-1290 upregulation and NFIX downregulation both correlated short overall and disease-free survivals of ESCC patients. Importantly, the prognostic value of combined miR-1290 and NFIX expression was more significant than those considered alone. CONCLUSIONS: Our data suggest that the dysregulation of miR-1290-NFIX axis may play crucial roles in esophageal carcinogenesis and progression. We also confirmed miR-1290 and its target gene NFIX as independent prognostic factors for ESCC patients.

Novel alternative splice variants of NFIX and their diverse mRNA expression patterns in dairy goat.

The nuclear factor I/X (NFIX) is a member of NFI family and contributes to muscle and brain development. Numerous genes coding for alternative splicing isoforms play potential but different roles in the biological process. To date, transcript variants of NFIX gene and their expression profiles have never been elucidated in dairy goat. Herein, we identified and verified the expression of two novel transcripts (NFIXa and NFIXb) of NFIX gene in dairy goat. Compared with the normal transcript (NFIX), the NFIXa variant lacked the first and ninth exons, while the NFIXb variant lacked the first, seventh and ninth exons; the NFIXa variant was 69 nt longer than the normal transcript in the 5' end site of the seventh exon, while the NFIXb variant was 66 nt longer in the 5' end site of the seventh exon. Quantitative real-time PCR results showed that the expression levels of the three variants were significantly different. The normal NFIX variant was abundantly expressed in the lungs, the NFIXa variant was highly expressed in the pancreas, and the NFIXb variant was abundantly expressed in both the lung and the pancreas. Additionally, the NFIXa variant showed a significantly higher expression level than those of the normal NFIX and the alternative NFIXb variants in the liver, spleen, adipose, intestine and the testis (P<0.01 or P<0.05), respectively. Expression of the NFIXa variant in the brain was significantly higher than that of the NFIXb variant (P<0.01). These findings suggest that the NFIXa isoform is the most abundant isoform in certain tissues of the dairy goat. This study represents the first report on alternative splicing variants of the goat NFIX gene and their expression profiles. It should help elucidate the function of NFIX gene in dairy goat.