RESUMEN
Long non-coding RNA has attracted the interest of researchers as a relevant factor that can influence human cancers. As an oncogene and suppressor gene, it has numerous pathways and is closely related to the pathophysiology of human diseases. Meanwhile, it may become a novel treatment option and target for tumor treatment. CRNDE is the gene symbol for Colorectal Neoplasia Differentially Expressed (non-protein-coding) since it was found to be considerably higher in colorectal cancer when it was first discovered. It's transcribed from human chromosome 16. Many studies have shown that it is intimately linked to the etiology of many tumors and malignancies. According to the paper, the biological function and pathophysiological mechanism of CRNDE in tumors have been studied extensively in recent years. PubMed served as an essential platform for conducting literature searches and related analyses. CRNDE, a long non-coding RNA closely related to tumors, was highly expressed in many tumor cells. There were various underlying mechanisms affecting the progression of CRNDE-regulated tumorigenesis, including hepatocellular carcinoma, gastric cancer, prostate carcinoma, oral squamous cell carcinoma, breast cancer, thyroid cancer, myeloma, leukemia, melanoma, colorectal cancer, glioblastoma, osteosarcoma, cervical cancer, intrahepatic cholangiocarcinoma, nonsmall cell lung cancer, hepatoblastoma cell tumor, abdominal aortic aneurysm, nasopharyngeal carcinoma, bladder cancer, Wilms tumor, medulloblastoma, pancreatic cancer, gallbladder cancer, ovarian cancer, and renal cell carcinoma. CRNDE is involved in the processes of proliferation, migration, invasion, and inhibition of apoptosis of various cancer cells.
Asunto(s)
Carcinoma de Pulmón de Células no Pequeñas , Carcinoma de Células Escamosas , Neoplasias Colorrectales , Neoplasias Hepáticas , Neoplasias Pulmonares , MicroARNs , Neoplasias de la Boca , ARN Largo no Codificante , Masculino , Humanos , Carcinoma de Pulmón de Células no Pequeñas/patología , ARN Largo no Codificante/genética , Carcinoma de Células Escamosas/genética , Línea Celular Tumoral , Neoplasias Pulmonares/patología , Neoplasias de la Boca/genética , Neoplasias Hepáticas/patología , Proliferación Celular/genética , Regulación Neoplásica de la Expresión Génica , MicroARNs/metabolismoRESUMEN
Treatment for epilepsy, particularly temporal lobe epilepsy, is challenging. Baicalein has multiple effects, including anti-inflammatory action. However, little is known about its efficacy in treatment of epilepsy. In this study, we established a pilocarpine-induced rat model and used it for assessment of baicalein efficacy in vivo. We predicted the pharmacological mechanism of baicalein by network pharmacology and RNA sequencing analyses. Pilocarpine epileptic rats treated with baicalein exhibited improved average seizure severity, seizure frequency, seizure duration, and survival time. Network pharmacology and RNA sequencing identified the differentially expressed genes between the baicalein treatment and epileptic groups. Insulin-like growth factor 1 receptor (IGF1R) was chosen as the top candidate target because of its overlapping findings in RNA sequencing and network pharmacology data. Western blotting, immunofluorescence, and polymerase chain reaction analyses showed that baicalein inhibited microglial proliferation, IGF1R, and inflammatory cytokine expression. Moreover, baicalein improved epilepsy symptoms. Inhibition of IGF1R function by blocking with AXL1717 enhanced baicalein treatment efficacy both in vivo and in vitro. In conclusion, baicalein exerted antiepileptic effects by regulation of IGF1R in a pilocarpine-induced rat model.
