Abstract. Whole genome transcriptomic analyses have identified a large number of long non-coding RNAs (lncRNAs), many of which are involved in a variety of biological functions. However, their functions and molecular mechanisms associated with prostate cancer (PCa) progression to a virulent and androgen-independent (AI) form remain elusive. Herein, we investigated the lncRNA expression profiles of the indolent, androgen-dependent (AD) LNCaP cell line to the aggressive metastatic, AI C4-2 cell line using microarray technology. The differentially expressed lncRNAs and genes were identified by microarray technology and the association in cis or in trans was analyzed to find potential lncRNA target genes. Expression of candidate lncRNAs and putative targets was evaluated by real-time quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The functions of linc00963 on cell proliferation, apoptosis, migration and invasion were evaluated by a knockdown strategy in vitro using MTT, flow cytometric analysis and transwell chamber assays. lncRNAs (n=134) were differentially expressed (FDR <0.001 and fold change ≥2) between the LNCaP and C4-2 cell lines. Linc00963 was upregulated most obviously evaluated by qRT-PCR. Knockdown of linc00963 attenuated C4-2 cell proliferation, motility, invasion ability, the expression of EGFR and phosphorylation levels of AKT, and promoted cell apoptosis. Linc00963 was involved in the prostate cancer transition from androgendependent to androgen-independent and metastasis via the EGFR signaling pathway.

Neutrophils have been found to play an important role in the pathogenesis of inflammatory bowel disease (IBD), and anti-TNF-α mAb (i.e., infliximab) therapy is demonstrated to be effective in the induction of clinical remission and mucosal healing in these patients. However, how anti-TNF-α mAb regulates the functions of neutrophils is still unknown. Herein, we found that anti-TNF-α therapy significantly downregulated infiltration of neutrophils in inflamed mucosa of IBD patients. Importantly, anti-TNF-α mAb could inhibit neutrophils to produce proinflammatory mediators, such as ROS, calprotectin, IL-8, IL-6, and TNF-α. These data indicate that TNF-α plays a critical role in the induction of mucosal inflammatory response, and that blockade of TNF-α modulates intestinal homeostasis through balancing immune responses of neutrophils.

Age, severity of brain injury, neuroimaging results, treatment methods, and early-stage seizures are independent risk factors of PTE.

No abstract