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Cervical cancer (CC) is a type of pelvic malignant tumor that severely threatens women's health. Current evidence suggests that IER5, as a potential radiosensitizer, promotes irradiation-induced apoptosis in CC tissues in patients undergoing chemoradiotherapy. IER5 has been shown to be involved in the G2/M-phase transition. In the present study, we used Cdc25B as the breakthrough point to explore the underlying mechanism of IER5 in the cell cycle regulation of radiation-damaged HeLa cells. IER5 was evidently upregulated after irradiation, but Cdc25B was significantly downregulated. In monoclonal IER5-silenced HeLa cells, irradiation-induced downregulation of Cdc25B was attenuated. The effect of irradiation on Cdc25B promoter activity was determined by dual-luciferase reporter assays. The response elements on the Cdc25B promoter related to irradiation were predicted by JASPAR. These conserved sequences were mutated individually or in combination by splicing-by-overlap extension PCR, and their function was confirmed by dual-luciferase reporter assays. The enrichment efficiency of transcription factors after irradiation was determined by chromatin immunoprecipitation (ChIP) assay. Both Sp1/Sp3 and NF-YB binding sites were involved in irradiation-mediated regulation of Cdc25B. IER5 was involved in irradiation-mediated regulation of Cdc25B through the NF-YB binding site. Furthermore, ChIP assays showed that IER5 bound to the Cdc25B promoter, and the binding of IER5 to the Cdc25B promoter region in irradiation-induced HeLa cells induced the release of the coactivator p300 through interaction with NF-YB. Taken together, these findings indicate that IER5 is the transcriptional repressor that accelerates the downregulation of Cdc25B expression after irradiation.

Sprague Dawley rats were exposed to beryllium sulfate (BeSO4), and proteomic and bioinformatic techniques were applied to screen for differentially expressed proteins in their lung tissue and serum. A total of 12 coexpression modules were constructed for 18 samples with 2333 proteins. Four modules were found to have significant differences in the regulation of protein coexpression modules in the serum following exposure to BeSO4. A further three modules had significant differences in the regulation of protein coexpression modules in the lung tissues. Five modules with good correlation were obtained by calculating the gene significance and module membership values, whereas these module Hub proteins included: Hspbp1, Rps15a, Srsf2, Hadhb, Elmo3, Armt1, Rpl18, Afap1L1, Eif3d, Eif3c, and Rps3. The five proteins correlating highest with the Hub proteins in the lung tissue and serum samples were obtained using string analysis. KEGG and GO enrichment analyses showed that these proteins are mainly involved in ribosome formation, apoptosis, cell cycle regulation, and tumor necrosis factor regulation. By analyzing the biological functions of these proteins, proteins that can be used as biomarkers, such as Akt1, Prpf19, Cct2, and Rpl18, are finally obtained.

The specific cytotoxic effect of nanoparticles on tumor cells may be used in future antitumor clinical applications. Silver nanoparticles (AgNPs) have been reported to have potent cytotoxic effect, but the mechanism is unclear. Here, AgNPs were synthesized, and the particle average size was 63.1 ± 8.3 nm and showed a nearly circular shape, which were determined by transmission electron microscopy and field emission scanning electron microscopy. The selected area electron diffraction patterns showed that the nanoparticles were crystalline. The energy-dispersive X-ray spectrum proved that silver is the main component of nanoparticles. The AgNPs showed potent cytotoxicity in breast cancer cells, no matter whether they were tamoxifen sensitive or resistant. Next, we found that a long noncoding RNA, XLOC_006390, was decreased in AgNPs-treated breast cancer cells, coupled to inhibited cell proliferation, altered cell cycle and apoptotic phenotype. Downstream of AgNPs, XLOC_006390 was recognized to target miR-338-3p and modulate the SOX4 expression. This signaling pathway also mediates the AgNPs function of sensitizing tamoxifen-resistant breast cancer cells to tamoxifen. These results provide a new clue for the antitumor mechanism of AgNPs, and a new way for drug development by using AgNPs.

To study the extraction technology of polysaccharides (AAP) from Chinese herbal medicine formula and its mechanism of delaying aging. First, L9(3)4 orthogonal test was used to optimize the optimal enzyme-assisted extraction parameters of polysaccharides. And the anti-aging effects was evaluated by detecting mitochondrial function, protein, DNA, adhesion molecules and cell cycle in aging rats. The optimal extraction process parameters were the cellulase concentration of 1.5%, the pH at 5, the enzyme temperature at 50°C and the extraction time of 180 min. The anti-aging results showed that AAP can effectively increase the activities of malate dehydrogenase, succinate dehydrogenase and superoxide dismutase. It also can decrease the activity of monoamine oxidase and methane dicarboxylic aldehyde levels in the brain tissue. Meanwhile, the polysaccharides enhanced telomerase activity while reduced p16 protein expression of the brain mitochondria. In addition, the polysaccharides continued to improve heart damage and significantly lessen mitochondrial DNA concentrations. For a certain period of time, it also enhanced the activity of superoxide dismutase, reduced glutathione, glutathione peroxidase and decreased protein carbonyl and methane dicarboxylic aldehyde content of kidney in D-galactose-induced aging rats. Furthermore, the polysaccharides restored the number of cells in the peripheral blood lines and BMNC through inhibiting the drop of the number of red blood cells, white blood cells, platelets in the peripheral blood and bone marrow mononuclear cell of the aging rats. At the same time, AAP accelerated G1 phase cell to enter S phase in cell cycle in aging rats. Our research suggests that the polysaccharides may be a potential anti-aging agent and can be further developed as a functional food or new drug to delay aging or treat aging-related diseases.

OBJECTIVES: The aim of the study was to correlate the Ki-67 and cyclin A labelling index (LI) with clinical characteristics and risk of recurrence of craniopharyngiomas. METHODS: 47 consecutive patients were studied, 21 female and 26 male, aged 34.3 (2.8) years. Immunohistochemical analysis was performed on paraffin wax embedded material using monoclonal antibodies directed against the proliferation associated nuclear antigen Ki-67 and cyclin A. RESULTS: The median Ki-67 LI was 8.6% (interquartile range, 4.4%-14.0%). Ki-67 LI was significantly higher in tumours with a heavy inflammatory reaction and diabetes insipidus at presentation, whereas other clinical and histological features were not associated with the proliferation index. There was a strong linear correlation between Ki-67 LI and cyclin A LI (r = 0.77; p

Biologists have long been interested in both the regularities and the deviations in the relationship between brain, development, ecology, and behavior between taxa. We first examine some basic information about the observed ranges of fundamental changes in developmental parameters (i.e. neurogenesis timing, cell cycle rates, and gene expression patterns) between taxa. Next, we review what is known about the relative importance of different kinds of developmental mechanisms in producing brain change, focusing on mechanisms of segmentation, local and general features of neurogenesis, and cell cycle kinetics. We suggest that a limited set of developmental alterations of the vertebrate nervous system typically occur and that each kind of developmental change may entail unique anatomical, functional, and behavioral consequences for the organism. Thus, neuroecologists who posit a direct mapping of brain size to behavior should consider that not any change in brain anatomy is possible.

From the yeastCandida utilis a compound was isolated which uncouples the process of cell growth and division by accelerating the cell division without influencing outgrowth of cell mass when applied on another population of identical yeasts. This compound accelerated the initiation of DNA synthesis and had no influence on the synthesis of RNA and protein. Moreover, in the presence of division inducing factor the yeasts started multiplication before the content per cell reached the control level. The stimulating effect of division inducing factor was not obvious when the proteosynthesis of yeast cells was inhibited. We concluded that the division inducing factor regulates the formation of a protein which is synthesized in a very small amount and has a role in the initiation of DNA replication.