RESUMO
The incidence of malignant tumors is increasing year by year. Early detection and diagnosis of malignant tumors can improve the prognosis of patients and prolong their life. Pathological biopsy is the current gold standard for diagnosis, but the results of pathological biopsy are affected by the sampling site and cannot fully reflect the nature of the disease. Moreover, the invasive nature of pathological biopsy limits repeated detection. Liquid biopsies are non-invasive and can be used for early detection and monitoring of tumors, which considered to represent a promising tool. Platelets make themselves to be one of the richest liquid biopsy sources by the capacity to take up proteins and nucleic acids and alter their megakaryocyte-derived transcripts and proteins in response to external signals, which are called tumor-educated platelets (TEPs). In this article, we will review the application of tumor-educated platelets in various malignancies (nasopharyngeal carcinoma, prostate cancer, lung cancer, glioblastoma, colorectal cancer, pancreas cancer, ovarian cancer, sarcoma, breast cancer and hepatocellular carcinoma) and provide theoretical basis for the research of TEPs in tumor diagnosis, monitoring and treatment.
Assuntos
Neoplasias da Mama , Neoplasias Hepáticas , Neoplasias Pulmonares , Masculino , Humanos , Neoplasias Pulmonares/patologia , Biópsia Líquida/métodos , Neoplasias da Mama/patologia , Plaquetas/patologia , Biópsia , Neoplasias Hepáticas/patologia , Biomarcadores Tumorais/metabolismoRESUMO
Antibacterial monomers incorporated in dentin bonding systems may have toxic effects on the pulp. Thus, the cytotoxicity of antibacterial monomers and its underlying mechanisms must be elucidated to improve the safety of antibacterial monomer application. The influence of an antibacterial monomer, methacryloxylethyl cetyl ammonium chloride (DMAE-CB), on the vitality of L929 mouse fibroblasts was tested using MTT assay. Cell cycle progression was studied using flow cytometry. Production of intracellular reactive oxygen species (ROS) after DMAE-CB treatment was measured using 2,7-dichlorodihydrofluorescein diacetate staining and flow cytometry analysis. Loss of mitochondrial membrane potential, disturbance of Bcl-2 and Bax expression, as well as release of cytochrome C were also measured using flow cytometry analysis or Western blot to explore the possible involvement of the mitochondrial-related apoptotic pathway. DMAE-CB elicited cell death in a dose-dependent manner and more than 50 percent of cells were killed after treatment with 30 µM of the monomer. Both necrosis and apoptosis were observed. DMAE-CB also induced G1- and G2-phase arrest. Increased levels of intracellular ROS were observed after 1 h and this overproduction was further enhanced by 6-h treatment with the monomer. DMAE-CB may cause apoptosis by disturbing the expression of Bcl-2 and Bax, reducing the mitochondrial potential and inducing release of cytochrome C. Taken together, these findings suggest that the toxicity of the antibacterial monomer DMAE-CB is associated with ROS production, mitochondrial dysfunction, cell cycle disturbance, and cell apoptosis/necrosis.