LncRNA NORAD promotes thyroid carcinoma progression by targeting miR-451.

OBJECTIVE: Long non-coding RNA (lncRNA) NORAD plays an essential role in the development and progress of papillary thyroid carcinoma (PTC). MicroRNA-451 (MiR-451) has been identified as playing an inhibitory role in some types of cancer. However, the molecular mechanism of lncRNA NORAD regulating metastasis of PTC cells by miR-451 has not been fully elucidated. MATERIALS AND METHODS: Real-Time quantitative Polymerase Chain Reaction (RT-qPCR) or Western blot analysis of the expression of NORAD, miR-451, and interleukin-6 receptor (IL-6R) in PTC cell lines were carried out. The detection of Luciferase reporter gene showed the relationship between lncRNA NORAD, miR-451 and IL-6R. Cell Counting Kit-8 (CCK-8) assay and transwell assay were performed to detect the influence of lncRNA NORAD, miR-451 on the proliferation, migration, and invasion of PTC cells. RESULTS: The results of RT-qPCR and Western blotting suggested that the expression of lncRNA NORAD and IL-6R were higher than that of the control group, while the expression of miR-451 was lower. Transwell assay indicated that the knockdown of lncRNA NORAD or overexpression of miR-451 significantly inhibited cell proliferation, migration and invasion in PTC cell lines. In addition, lncRNA NORAD negatively controls the expression of miR-451, resulting in the upregulation of IL-6R. IL-6R overexpression can reverse the inhibitory effect of lncRNA NORAD knockdown or miR-451 on PTC cell proliferation and metastasis. CONCLUSIONS: Our results indicated that the cell migration and invasion were inhibited by knockdown of lncRNA NORAD or overexpression of miR-451, suggesting that the axis of lncRNA NORAD -miR-451- IL-6R was involved in the development of PTC.

MiR-526b suppresses cell proliferation, cell invasion and epithelial-mesenchymal transition in breast cancer by targeting Twist1.

OBJECTIVE: The aberrant expression of microRNAs (miRNAs) acts as crucial regulators in the tumorigenesis of breast cancer (BC). The aim of the study is to investigate the functional effects of miR-526b expression in breast cancer progression. PATIENTS AND METHODS: The expression level of miR-526b in breast cancer tissues and cell lines was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation, migration, and invasion capacity was detected by CCK-8 cell proliferation, colony formation, and transwell invasion assays after up-regulating or down-regulating miR-526b expression in breast cancer cells. Bioinformatics analysis and Dual-Luciferase reporter gene assays were used to demonstrate that Twist1 was a target of miR-526b. Western blot analysis was also performed. RESULTS: We showed that miR-526b expression was significantly downregulated in breast cancer tissues compared to adjacent normal tissues. Lower miR-526b expression was associated with lymph node metastasis in breast cancer patients. Function assays showed that upregulation of miR-526b expression suppressed cell proliferation, cell colony formation, and cell invasion ability in breast cancer. Furthermore, the upregulation of miR-526b suppressed EMT makers Vimentin expression but increased the E-cadherin expression. Mechanically, we showed that miR-526b inhibited cell EMT process by targeting Twist1 expression. CONCLUSIONS: Thus, our evidence indicated that miR-526b may serve as a potential target of breast cancer treatment.

Loss of CD23 is a consequence of B-cell activation. Implications for the analysis of B-cell lineages.

When splenic CD5- B cells are stimulated with antiimmunoglobulin they become CD5+ and have a prolonged in vitro life. Further treatment with IL-6 induces a loss of surface CD23 and IgD; that is, they resemble freshly isolated peritoneal CD5+ cells. These data suggest that the CD5 phenotype is induced after sIg-mediated B-cell activation. Additional support for this view arises from the observation that the loss of CD23 and IgD can be induced by another activation inducer, LPS, although in this case CD5 is not expressed. Thus, activation by anti-Ig plus IL-6 or by LPS induces CD23 loss. Consistent with the hypothesis that the loss of CD23 is a consequence of activation, we now report that the surface expression of CD23 varies inversely with the amount of total cellular RNA. We also find both CD23 positive and negative B cells among freshly isolated splenic CD5- B cells. In young mice a proportion of small splenic CD5+ B cells are CD23+, providing additional evidence that CD23 is present on all B cells prior to activation. A comparison of the features of CD5+ B cells and the antibody responses to thymus-dependent and thymus-independent antigens leads us to hypothesize that the CD5 phenotype arises as a consequence of thymus-independent type 2 (TI-2) stimulation. The relationship of CD5 expression to B-cell lineage (fetal vs. adult bone marrow) is discussed.

Treatment of murine CD5- B cells with anti-Ig, but not LPS, induces surface CD5: two B-cell activation pathways.

Anti-Ig stimulated murine B cells express high levels of surface CD5 (ly-1) and increased CD44 while maintaining surface IgD, CD23 and J11d. Sorting of CD5- and CD5+ cells demonstrates that anti-Ig induces CD5 expression rather than the selective expansion of CD5+ cells. Anti Ig plus interleukin-6 (IL-6) induces the CD23, IgD, low ly-5 (B220) (CD45low), J11dhigh phenotype of typical CD5+ peritoneal B cells. In contrast, lipopolysaccharide (LPS)-stimulated B cells have high levels of CD44 but decreased surface IgD, CD23 and J11d and no CD5. Thus LPS and anti-Ig generate activated cells with differing phenotypes. Induced CD5+ cells have increased viability, even in the absence of added exogenous factors, while the viability of CD5- B cells is dependent on factors such as IL-4. We conclude that conventional CD5- B cells can be activated by either of two pathways: one generating CD5+ B cells; the other yielding conventional activated cells. We hypothesize that the first path requires slg cross-linking and corresponds to T-independent (type 2) stimulation, while cognate interaction with helper T cells in the absence of slg cross-linking induces B cells to enter the second path.

Studies on the origin of the follicle associated epithelial cells of bursa Fabricii.

The present paper, by using interspecific chimera of chick and quail and submicroscopic study on the bursal follicle associated epithelium (FAE) cells during differentiation, indicates that FAE cells of the bursa of Fabricius are formed not by differentiation of the epithelial cells but originate from the mesenchymal cells after invading the bursal anlage, and then differentiate into FAE cells. A new suggestion is given on the interpretation of the mechanism of the invasion of hemopoietic stem cells into the bursal epithelium.