Background
MicroRNAs (miRNAs) and Twist1-induced epithelial-mesenchymal transition (EMT) in cancer cell dissemination are well established, but the involvement of long noncoding RNAs (lncRNAs) in Twist1-mediated signaling remains largely unknown.
Methods
RT-qPCR and western blotting were conducted to detect the expression levels of lncRNA JPX and Twist1 in lung cancer cell lines and tissues. The impact of JPX on Twist1 expression, cell growth, invasion, apoptosis, and in vivo tumor growth were investigated in lung cancer cells by western blotting, rescue experiments, colony formation assay, flow cytometry, and xenograft animal experiment.
Results
We observed that lncRNA JPX was upregulated in lung cancer metastatic tissues and was closely correlated with tumor size and an advanced stage. Functionally, JPX promoted lung cancer cell proliferation in vitro and facilitated lung tumor growth in vivo. Additionally, JPX upregulated Twist1 by competitively sponging miR-33a-5p and subsequently induced EMT and lung cancer cell invasion. Interestingly, JPX and Twist1 were coordinately upregulated in lung cancer tissues and cells. Mechanically, the JPX/miR-33a-5p/Twist1 axis participated in EMT progression by activating Wnt/β-catenin signaling.
Conclusions
These findings suggest that lncRNA JPX, a mediator of Twist1 signaling, could predispose lung cancer cells to metastasis and may serve as a potential target for targeted therapy.
MicroRNAs (MiRNAs) have been found to be dysregulated in lung cancer tissues compared to their matched paracancerous tissues. However, the roles of miRNAs in peripheral blood as potential biomarkers for early diagnosis of lung cancer remain poorly understood. Here we found that miR-33a-5p and miR-128-3p were down-regulated in lung cancer tissues and cell lines. The expression levels of miR-33a-5p and miR-128-3p in lung cancer tissues were significantly correlated to TNM stages. MiR-128-3p in lung cancer tissues was also remarkably related to smoking and tumor size. The relative expression levels of miR-33a-5p and miR-128-3p were positively correlated in lung cancer tissues. Notably, miR-33a-5p and miR-128-3p in whole blood of lung cancer patients or early-stage lung cancer patients (TNM stage I-II) were lowly expressed as compared with that in healthy controls. The receiver operating characteristic curve (ROC) analyses revealed higher area under the ROC curve (AUC) values and higher sensitivity/specificity of miR-33a-5p and miR-128-3p alone and in combination were superior to that of traditional tumor markers (CYFR21-1, NSE and CA72-4). Importantly, both miR-33a-5p and miR-128-3p in whole blood were highly stable even under different harsh conditions. The results demonstrate that tumor suppressor miR-33a-5p/miR-128-3p in whole blood can serve as novel biomarkers for the early detection of lung cancer.
BackgroundCopy number variants contribute to genetic variation in birds. Analyses of copy number variants in chicken breeds had focused primarily on those from commercial varieties with nothing known about the occurrence and diversity of copy number variants in locally raised Chinese chicken breeds. To address this deficiency, we characterized copy number variants in 11 chicken breeds and compared the variation among these breeds.ResultsWe presented a detailed analysis of the copy number variants in locally raised Chinese chicken breeds identified using a customized comparative genomic hybridization array. We identified 833 copy number variants contained within 308 copy number variant regions. The median and mean sizes of the copy number variant regions were 14.6 kb and 35.1 kb, respectively. Of the copy number variant regions, 138 (45%) involved gain of DNA, 159 (52%) involved loss of DNA, and 11 (3%) involved both gain and loss of DNA. Principal component analysis and agglomerative hierarchical clustering revealed the close relatedness of the four locally raised chicken breeds, Shek-Ki, Langshan, Qingyuan partridge, and Wenchang. Biological process enrichment analysis of the copy number variant regions confirmed the greater variation among the four aforementioned varieties than among the seven other breeds studied.ConclusionOur description of the distribution of the copy number variants and comparison of the differences among the copy number variant regions of the 11 chicken breeds supplemented the information available concerning the copy number variants of other Chinese chicken breeds. In addition to its relevance for functional analysis, our results provided the first insight into how chicken breeds can be clustered on the basis of their genomic copy number variation.
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