35 research outputs found
PLAC8 Overexpression Promotes Lung Cancer Cell Growth via Wnt/β-Catenin Signaling
No full textThe PLAC8 expression in lung cancer tissues and in vitro grown lung cancer cells, as well as the involvement of the Wnt/β-Catenin signaling pathway, was investigated in this process. PLAC8 protein expression in human lung cancer tissues and lung tumor cells of different strains was discovered using immunohistochemistry staining and Western blot, respectively. Animal models of PLAC8 overexpression and knockdown were created using lentivirus. The development in tumor tissue was seen both in vitro and vivo. The Wnt/β-Catenin signaling pathway played an important part in this process, as shown by the dual luciferase reporter gene system. PLAC8 expression was elevated in lung cancer tissues and plasma and decreased in plasma after lung tumor resection. PLAC8 upregulation promotes cell proliferation in vivo and in vitro, while PLAC8 downregulation inhibits cell viability and proliferation. The results of the dual luciferase reporter gene system suggest that PLAC8 can significantly activate the Wnt/β-Catenin signaling pathway in cells and can conduct signaling through it. A potential treatment targeting the prognosis of lung cancer patients may be PLAC8 overexpression, which promotes the lung cancer cell proliferation through controlling the Wnt/β-Catenin signaling pathway
Electric field modulated conduction mechanism in Al/BaTiO3/La0.67Sr0.33MnO3 heterostructures
No full textMediating a metastable state is a promising way to achieve a giant modulation of physical properties in artificial heterostructures. A metastable state La0.67Sr0.33MnO3 (LSMO) layer suffering tensile strain was grown on MgO substrates. Incorporating with the ferroelectric BaTiO3 (BTO) layer, an accumulation or depletion state controlled by electric fields can be formed at the BTO/LSMO interface, which drives a switching of the conduction mechanism between space charge limited conduction and Poole-Frenkel emission, corresponding to the low and high resistance states. Our results lighten an effective way for electric-field modulated resistance states in multiferroic magnetoelectric devices.This work was supported by the National Natural Science Foundation of China (51272174 and 11434006). The authors thank S. Wu and L. Y. Xu for PFM and KPFM performance. This work was supported by Beijing Synchrotron Radiation Facility (BSRF)
The Function and Molecular Mechanism of Commensal Microbiome in Promoting Malignant Progression of Lung Cancer
No full textThe human commensal microbiome existing in an internal environment is relatively consistent with that of the host. The presence of bacterial dysbiosis, on the other hand, promptly results in the termination of this symbiotic association. The altered microbial structure in the lung may be responsible for the development of lung cancer by controlling the host’s inflammatory response and influencing a variety of immunological pathways. More and more studies have pointed to the fact that the commensal microbiota plays a vital role in both the development of tumors and the body’s response to lung cancer treatment. Microbiome dysbiosis, genotoxicity, virulence effect, and epigenetic dysregulations are some of the potential mechanisms that may lie behind the process of tumorigenesis that is mediated by microbiome. Other potential mechanisms include regulating host immune activity through a variety of pathogenic factors, dysregulating host metabolism as a result of microbiome alterations, and microbiome dysbiosis. In this historical overview, we go through some of the more recent mechanistic discoveries into the biological processes that are involved in lung cancer that are caused by bacteria. Without a question, obtaining a greater knowledge of the dynamic link between the lung microbiome and lung cancer has the potential to inspire the development of innovative early detection and customized treatment methods for lung cancer
An in vitro assay to monitor sertoli cell blood-testis barrier (BTB) integrity
No full textIn this chapter, we detail a reliable, effective, and easy to perform assay to monitor the Sertoli cell blood–testis barrier (BTB) integrity. While the BTB in the testis is composed of the tight junction (TJ) barrier and basal ES (ectoplasmic specialization, a testis-specific actin-rich adherens junction (AJ) type), this method is applicable to all other blood–tissue barrier in vitro, including endothelial TJ-barrier of the blood–brain barrier (BBB). Furthermore, this method does not require expensive set up, and can be rapidly performed by any standard biochemistry/cell biology/molecular biology laboratory. The basic idea is built on the concept that a functional blood–tissue barrier, such as the BTB conferred by Sertoli cells in the testis, is capable of blocking the diffusion of a small membrane impermeable biotin (e.g., EZ-Link Sulfo-NHS-LC-biotin, Mr. 556.59) across the barrier. However, when this barrier is compromised, such as following treatment with a toxicant or knockdown of a relevant gene necessary to confer the TJ-barrier function, the biotin will permeate the barrier, reaching the Sertoli cell cytosol. Biotin can be subsequently visualized by using streptavidin conjugated to a fluorescence tag such as Alexa Fluor 488 (green fluorescence) which can be easily visualized by a standard fluorescence microscope
Tumor Microenvironment: Lactic Acid Promotes Tumor Development
No full textLactic acid is a “metabolic waste” product of glycolysis that is produced in the body. However, the role of lactic acid in the development of human malignancies has gained increasing interest lately as a multifunctional small molecule chemical. There is evidence that tumor cells may create a large amount of lactic acid through glycolysis even when they have abundant oxygen. Tumor tissues have a higher quantity of lactic acid than normal tissues. Lactic acid is required for tumor development. Lactate is an immunomodulatory chemical that affects both innate and adaptive immune cells' effector functions. In immune cells, the lactate signaling pathway may potentially serve as a link between metabolism and immunity. Lactate homeostasis is significantly disrupted in the TME. Lactate accumulation results in acidosis, angiogenesis, immunosuppression, and tumor cell proliferation and survival, all of which are deleterious to health. Thus, augmenting anticancer immune responses by lactate metabolism inhibition may modify lactate levels in the tumor microenvironment. This review will evaluate the role of lactic acid in tumor formation, metastasis, prognosis, treatment, and histone modification. Our findings will be of considerable interest to readers, particularly those engaged in the therapeutic treatment of cancer patients. Treatments targeting the inhibition of lactate synthesis and blocking the source of lactate have emerged as a potential new therapeutic option for oncology patients. Additionally, lactic acid levels in the plasma may serve as biomarkers for disease stage and may be beneficial for evaluating therapy effectiveness in individuals with tumors
Polyethylene Glycol Loxenatide (PEX-168) Reduces Body Weight and Blood Glucose in Simple Obese Mice
No full textBackground. At present, there is a lack of drug treatment for obese patients, so it is needed to find a drug that is effective and has few side effects to treat obesity. PEX-168 is a novel long-acting glucagon-like peptide-1 receptor agonist for T2DM. It improves blood glucose with fewer side effects. The aim of the present study was to investigate the effect of PEX-168 on blood glucose and body weight of mice with simple obesity. Methods. Thirty healthy and 6-week-old C57BL/6 male mice were randomly divided into a normal control group (NC, n = 6) and obesity model group (n = 24). The obesity model mice were randomly divided into a high-fat diet group (HF) and intervention groups with different doses of PEX-168 (0.03 mg/kg, 0.1 mg/kg, and 0.3 mg/kg). Each group includes 6 mice. Body weight, food intake, and fasting blood glucose (FBG) were evaluated after intraperitoneal injection, and the intervention was performed weekly for 12 weeks. Fasting insulin (FINS) levels were measured at the 12th week. Results. Compared with HF, the food intake of mice in the intervention groups decreased transiently, but there was no difference between different doses (P>0.05). The body weight of mice in the middle and high dose of PEX-168 intervention groups decreased significantly, and the differences were statistically significant (P0.05). At the 10th week, the incidence of transient hypoglycemia was 67% and 50% in the middle- and high-dose groups, respectively. The levels of serum FINS in the intervention groups were significantly lower than those in the HF group, and the differences were statistically significant (P0.05). Conclusions. PEX-168 showed significant improvement in the FBG and FINS levels of simple obese mice. Middle and high doses of PEX-168 could reduce the weight of simple obese mice, but there was a certain risk of hypoglycemia
Abstract A001: Colorectal cancer cell-derived exosomes containing miR-183-5p regulate angiogenesis via FOXO1
No full textDevelopment characteristics and potential of fault-fracture reservoir in southwest margin of Ordos Basin
No full textThe southwest margin of Ordos Basin has developed faults and fractures to varying scales, significantly enhancing the permeability of tight reservoirs and forming high-quality fault-fracture reservoirs against a backdrop of low permeability reservoir types. However, this also complicates the reservoir's homogeneity and the variability of its capacity, posing challenges for fine characterization of the reservoir's internal structure and for researching capacity control factors. To address these issues, the study employs spatial characterization of the fracture system, fracture classification, and capacity comparative analysis. Further, the development characteristics of the fault-fracture reservoir are defined through joint well-seismic and reservoir research. Key findings from this research include: 1） Establishment of the “binary four zones” model for fault-fracture reservoirs, which divides the reservoir into four distinct zones: the core fracture zone, the induced fracture zone, the micro-fracture transformation zone, and the matrix pore zone. Among these, the core fracture zone is identified as the primary contributor to production yield. 2） It is observed that the longer the fault extension length and the higher the solid drilling structure position, the higher the single well production capacity in the core fracture zone. The induced fracture zone's proximity to the fault correlates with higher production capacity, demonstrating the spatial impact of fault structures on reservoir productivity. 3） The production characteristics of fracture wells are categorized into three stages: ① the fracture system acts as the high yield stage; ② the fracture system serves as the storage stage and plays the role of diversion; ③ the fracture's primarily function in diversion. This research significantly increases the proportion of high-yield wells in the fault-fracture reservoir, providing crucial insights for guiding efficient, ongoing exploration and development activities in the Mesozoic reservoirs on the southwest margin of the basin. This strategic approach enhances understanding and management of fault-fracture reservoirs, optimizing resource extraction and improving operational efficiencies
Downregulation of microRNA-448 improves isoflurane-induced learning and memory impairment in rats
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