Aberrant expression through 3'UTR alternative polyadenylation in breast cancers.

Ki-67 (MKI67) is a marker of cellular proliferation of cancer. Here, we show that Ki-67 is post-transcriptionally regulated through alternative polyadenylation (APA) and microRNAs in breast cancer. We show that shortening of the 3'UTR results in the loss of the binding sites for the suppressive miRNAs and thus renders the transcript with a shortened 3'UTR insusceptible to miRNA-mediated suppression.

Differential expression of miR16 in glioblastoma and glioblastoma stem cells: their correlation with proliferation, differentiation, metastasis and prognosis.

The function of miR16 in multiforme glioblastoma multiforme (GBM) and its stem cells (GSCs) remains elusive. To this end, we investigated the patterns of miR16 expression in these cells and their correlation with malignant behaviors and clinical outcomes. The levels of miR16 and its targeted genes in tumor tissue of GBM and GBM SGH44, U87, U251 cells as well as their stem cell counterparts were measured by qRT-PCR or western blot or immunohistochemistry.

High expression of long noncoding RNA HULC is a poor predictor of prognosis and regulates cell proliferation in glioma.

Purpose: Emerging studies show that long noncoding RNAs (lncRNAs) have important roles in carcinogenesis. This study investigated the role of lncRNA highly upregulated in liver cancer (HULC) expression in glioma and its clinical significance in glioma patients.

Materials And Methods: HULC expression was detected in glioma tissues and cell lines by using real-time quantitative reverse transcription polymerase chain reactions.

miR128-1 inhibits the growth of glioblastoma multiforme and glioma stem-like cells via targeting BMI1 and E2F3.

MicroRNA128-1 (miR128-1), as a brain-specific miRNA, is downregulated in glioblastoma multiforme (GBM) and closely associated with the progression of GBM. However, the underlying molecular mechanism of the downregulation and its role in the regulation of tumorigenesis and anticancer drug resistance in GBM remains largely unknown. In the current study,we found that miR128-1 was downregulated in GBM and glioma stem-like cells (GSCs).