Objective In order to observe the effects of phenylace te (PA) on cells morphogeny during the process of inducing differentiation of glioma cell line C6. Methods After uranyl acetate staining,the change of ultrastruct ure of C6 cells before and after PA treatment was observed under transmission el etron microscopy. Results After PA treatment,the nuclear shape of C6 cell changed into regular and round like one from aberrant nucleus.In cytoplasm,there was s ignificant hyperplasia of endoplasmic reticulum (rER) which represents the degre e of cell differentiation. Conclusion PA could raise the differentiation degree of C6 cell at the subcellular level and decrease the malignant degree.
PURPOSE: To develop a model for studying cerebrovascular disease prevention in elderly women. METHODS: Sixty 18-month-old Sprague Dawley (SD) rats were randomly divided into an estrogen administration group (EA, n=30) and a non-administration group (NA, n=30); thirty 4-month-old SD rats were allocated to a control group. The EA group received estradiol benzoate starting on the 5th day of a 34-day breeding period, and the serum levels of estradiol (E2), estrogen receptor (ER), and malondialdehyde (MDA) were measured. The MCA of each group was then sampled for viscoelastic experiments. RESULTS: The serum levels of E2 and MDA in the EA group showed significant differences compared to those in the control group (p<0.05), while the difference in ER between the EA and control groups was not significant (p>0.05). The decrease in MCA stress at 7,200 s and the increase in strain at 7,200 s in the EA group showed no significant differences compared to the control group (p>0.05). CONCLUSION: Estradiol administration inhibited the formation of lipid peroxidation products and restored middle cerebral arterial viscoelasticity in aged female rats.
Glioblastoma, a notably aggressive brain tumor, is characterized by a brief survival period and resistance to conventional therapeutic approaches. With the recent identification of “Cuproptosis,” a copper-dependent apoptosis mechanism, this study aimed to explore its role in glioblastoma prognosis and potential therapeutic implications. A comprehensive methodology was employed, starting with the identification and analysis of 65 cuproptosis-related genes. These genes were subjected to differential expression analyses between glioblastoma tissues and normal counterparts. A novel metric, the “CP-score,” was devised to quantify the cuproptosis response in glioblastoma patients. Building on this, a prognostic model, the CP-model, was developed using Cox regression techniques, designed to operate on both bulk and single-cell data. The differential expression analysis revealed 31 genes with distinct expression patterns in glioblastoma. The CP-score was markedly elevated in glioblastoma patients, suggesting an intensified cuproptosis response. The CP-model adeptly stratified patients into distinct risk categories, unveiling intricate associations between glioblastoma prognosis, immune response pathways, and the tumor’s immunological environment. Further analyses indicated that high-risk patients, as per the CP-model, exhibited heightened expression of certain immune checkpoints, suggesting potential therapeutic targets. Additionally, the model hinted at the possibility of personalized therapeutic strategies, with certain drugs showing increased efficacy in high-risk patients. The CP-model offers a promising tool for glioblastoma prognosis and therapeutic strategy development, emphasizing the potential of Cuproptosis in cancer treatment.
The great importance of long noncoding RNAs (lncRNAs) has been acknowledged in tumorigenesis gradually. LncRNA LINC01857 is a novel lncRNA and has been reported to promote breast cancer progression. However, the biological roles of LINC01857 in glioma are not explored. In the present research, LINC01857 levels were found to be upregulated in glioma. In addition, LINC01857 expression is negatively correlated with survival rate in glioma patients. Functional investigation revealed that LINC01857 downregulation impaired glioma proliferation and invasiveness. Furthermore, LINC01857 knockdown led to repressed growth of glioma in vivo. We found that LINC01857 could be a sponge for miR-1281 and inhibits its level to upregulate TRIM65 expression. What's more, we showed that miR-1281 mimics also attenuated tumor cell proliferation, migration, and invasion. And rescue assays demonstrated that LINC01857 promotes glioma progression through modulating miR-1281/TRIM65 pathway. Collectively, this study first demonstrated that a novel LINC01857/miR-1281/TRIM65 signaling regulates glioma progression.
Glioma, an aggressive tumor in brain, presents a very poor prognosis. Emerging evidence has demonstrated that dysfunction of long noncoding RNAs (lncRNAs) is closely related to giloma development. However, the roles of lncRNA BLACAT1 in glioma are not unknown. In this study, we utilized in vitro and in vivo experiments to explore the effects of BLACAT1 on glioma cells. BLACAT1 levels were increased in glioma tissues. Upregulation of BLACAT1 showed poor prognosis. Silencing of BLACAT1 markedly repressed glioma proliferation, migration, and invasion, and suppressed glioma growth in vivo. We also illustrated that BLACAT1 worked as the sponge for miR-605-3p and promoted VASP expression. miR-605-3p was downregulated in glioma and repressed glioma proliferation, migration, and invasion. And VASP is upregulated and contributed to glioma progression. Summarily, this study highlights the important roles of BLACAT1/miR-605-3p/VASP axis in glioma progression.
Glioma is the most common form of malignant brain cancer with high mortality rate in human. Therefore, finding effective therapeutic strategy and revealing the underlying molecular mechanism is necessary. Ampelopsin (Amp), an effective component of the traditional Chinese herb of Ampelopsis grossedentata, is reported to have important biological properties, including anti-inflammatory, anti-cancer, and anti-oxidant activity; however, its effects on human glioma are poorly understood. Here, the in vitro and in vivo study was performed to investigate the anti-glioma ability of Ampelopsin. Human glioma cell lines of U251 and A172 were treated with Ampelopsin (0, 25, 50, and 100 uM) for 24 h, followed by various analysis. And human glioma xenograft models were established by injecting U251, accompanied with administration of Ampelopsin at 50 and 100 mg/kg to confirm the anti-cancer role of Ampelopsin. We found that Ampelopsin could suppress the glioma cell proliferation by modulating G1 and S phase arrest. Incubation with Ampelopsin led to the activity of Caspase-8, Caspase-9, Caspase-3 and poly (ADP-ribose) polymerases (PARP), indicating that Ampelopsin induced apoptotic response via both intrinsic and extrinsic signaling pathways. Additionally, autophagy was also observed in Ampelopsin-treated cancer cells, which is evidenced by autophagosome formation and LC3B-II accumulation. Ampelopsin-caused cancer cell death was obviously regained by apoptosis inhibitors. Further, Ampelopsin activated c-Jun N-terminal protein kinase (JNK) expression and enhanced reactive oxygen species (ROS) generation. Suppressing JNK markedly ameliorated Ampelopsin-induced apoptosis and autophagy, and ROS scavenger exhibited similar results. In vivo, Ampelopsin inhibited tumor growth and progression in mouse xenograft models. In conclusion, our findings indicated that Ampelopsin led to G1 and S phase arrest, triggered apoptosis and autophagy through potentiating ROS generation and JNK activation in human glioma cells. Thus, Ampelopsin might be a promising candidate against human glioma.
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