Abstract. Early reports suggest that nuclear factor IA (NFIA) is important in the pathogenesis of glioma. Our previous study demonstrated that the long non-coding RNA (lncRNA), RP5-833A20.1, suppressed the expression of NFIA in THP-1 macrophage-derived foam cells. However, the effect and possible mechanism of RP5-833A20.1 on glioma remains to be fully elucidated, and whether the NFIA-dependent pathway is involved in its progression has not been investigated. In the present study, the mechanisms by which RP5-833A20.1 regulates the expression of NFIA in glioma were investigated. The expression levels of RP5-833A20.1 and NFIA were determined in U251 cells and clinical samples using reverse transcription-quantitative polymerase chain reaction (PCR) analysis. The effects of RP5-833A20.1 on cell proliferation, invasion, cell cycle and apoptosis were evaluated using in vitro assays. The potential changes in protein expression were investigated using western blot analysis. The methylation status of the CpG island in the NFIA promoter was determined using bisulfite PCR (BSP) sequencing. It was found that the expression of RP5-833A20.1 was downregulated, whereas the expression of NFIA was upregulated in glioma tissues, compared with corresponding adjacent nontumor tissues from 20 patients with glioma. The overexpression of RP5-833A20.1 inhibited proliferation and cell cycle progression, and induced apoptosis in the U251 cells. The mRNA and protein levels of NFIA were markedly inhibited by overexpression of RP5-833A20.1 in the U251 cells. The overexpression of RP5-833A20.1 increased the expression of microRNA-382-5p in the U251 cells. The BSP assay revealed that the overexpression of RP5-833A20.1 enhanced the methylation level of the NFIA promoter. These results demonstrated that RP5-833A20.1 inhibited tumor cell proliferation, induced apoptosis and inhibited cell-cycle progression by suppressing the expression of NFIA in U251 cells. Collectively, these results indicated RP5-833A20.1 as a novel therapeutic target for glioma.
Decorin is widely understood to affect collagen fibrillogenesis. However, little is understood about its response to various mechanical loading conditions. In the present study, 36 Wistar rats were randomly divided into control (CON), moderate treadmill running (MTR) and strenuous treadmill running (STR) groups. Animals in the MTR and STR groups were subjected to a 4‑ or 8‑week treadmill running protocol. Subsequently, all Achilles tendons were harvested to perform histological and biochemical analyses. Decorin expression was markedly increased in the MTR group compared with the CON group at 4 and 8 weeks. Conversely, decorin expression was markedly decreased in the STR group compared with the CON and MTR group at 4 and 8 weeks. Furthermore, between the two time points, decorin expression levels were significantly increased in the MTR group, whereas they were markedly decreased in the STR group. These results suggested that MTR exercise may induce increased decorin expression via a balance of MMP‑2 and TIMP‑2, improving tendon structure and function. However, STR exercise may result in degradation of decorin due to an imbalance of MMP‑2 and TIMP‑2, with a bias to MMP‑2, resulting in a predisposition to tendinopathy.
Helitron transposons play an important role in host genome evolution due to their ability to capture genes and regulatory elements. In this study, we developed a pipeline to identify and annotate Helitrons systematically from 358 plant and 178 animal high‐quality genomes. All these data were organized into HelDB, a database where Helitrons can be explored with a user‐friendly Web interface and related software. Based on these data, further analysis showed that the number or the cumulative length of Helitrons is positively correlated with genome size. Helitrons had experienced two expansion periods in plants, with the first occurring 20–30 Ma and peaking at approximately 24 Ma. The second expansion occurred in the last 4 million years. The expansions might be due to stimulation of paleogeographic environment. Detailed investigation of gene capture by Helitrons in Brassicaceae and Solanaceae plants showed that the captured genes showed diverse functions. Interestingly, metal ion binding function was enriched in these captured genes in most species. This phenomenon might be due to the need for binding of divalent metal ions to the Rep domain required for Helitron transposition. This study improves our knowledge of the landscape and evolution of Helitron transposons in plants and paves a way for further functional studies of this kind of transposable element.
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