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Background The main pathological feature of silicosis is pulmonary fibrosis. Multiple miRNAs regulate the development of silicosis. Objective Using a fibroblast cell line, to explore the effect of miR-18a on the expression of extracellular matrix-related genes, and verify the mechanism. Methods The fibroblast cell line NIH-3T3 cells were transfected with miR-18a mimics or neurogenic locus notch homolog protein 2 (Notch2) small interfering RNA (siRNA). The mRNA expression changes of Acta2, Col1a1, and Notch2 were detected by real-time quantitative reverse transcription PCR (qRT-PCR), α-smooth muscle actin (α-SMA) and Notch2 were also detected at the protein level by Western blotting. To verify whether miR-18a could directly act on the complementary sequences of the Notch2 gene, human embryonic kidney HEK293T cells and the psiCHECKTM-2 vector were used. Results The results of qRT-PCR showed that in NIH-3T3 cells, the over-expression of miR-18a mimics for 36 h inhibited the mRNA expression of Col1a1 and Acta2 (P<0.05). The results of Western blotting showed that the protein expression abundance of α-SMA was decreased at 48 h of miR-18a mimics over-expression. The qRT-PCR results showed that the over-expression of miR-18a for 36 h had no significant effect on Notch2 gene expression, but the Western blotting results showed that the over-expression of miR-18a mimics inhibited the expression of Notch2 at the protein level. The results of the dual luciferase reporter vector assay showed that in HEK293T cells, both over-expressed miR-18a mimics and inhibitors for 24 h demonstrated that Notch2 is a direct target gene of miR-18a. When Notch2 was inhibited for 36 h, the qRT-PCR results showed that Acta2 and Col1a1 were down-regulated (P < 0.05), and the results of Western blotting showed that α-SMA protein was also inhibited. Conclusion The findings indicate that miR-18a could inhibit the expression of extracellular matrix-related genes of NIH-3T3 cells by directly acting on the 3’UTR of target gene Notch2.
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Glioma is one of the most common primary intracranial tumors, accounting for 80% of malignant brain tumors. The conventional treatment of glioma is surgical resection followed by temozolomide chemotherapy, but the drug resistance will gradually appear that results in a poor prognosis of the patient. Berberine is an alkaloid extracted from Coptis Rhizoma, which has a wide range of pharmacological activities. It exerts its pharmacological effects on glioma such as inhibiting tumor growth through controlling different molecular and cellular pathways. In this article, the application of berberine in the treatment of glioma and the research progress of specific molecular mechanism are reviewed.
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The application of biological technology and the deepening of tumor research have effectively improved the level of tumor diagnosis, treatment and clinical outcome prediction. However, the specific mechanisms of tumorigenesis and development are still unclear, and tumor drug resistance has also become an urgent problem that needs to be solved to improve the clinical outcome of patients. Considerable studies have shown that the extrachromosomal DNA (ecDNA) can promote tumorigenesis, development and drug resistance. EcDNA is a looser, rounded form of DNA with unique genetic properties that carry specific genes and regulatory elements. This paper will discuss the biological characteristics, tumor-promoting mechanisms and drug resistance-facilitating of ecDNA.
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Glioma is one of the most common and invasive malignant tumors in the central nervous system. The Wnt-β-catenin signaling pathway is a classical Wnt pathway, which is involved in the occurrence and development of glioma and other tumors. Long non-coding RNA (LncRNA) is a functional RNA molecule without protein coding function, which plays a regulatory role in the occurrence and development of various tumors. Recent studies have shown that LncRNA and Wnt-β-catenin signaling pathways are jointly involved in glioma growth, invasion, migration and other processes, but the complex mechanism has not been thoroughly elaborated. In this paper, the influence of Wnt-β-catenin signaling pathway and its related LncRNA on glioma was reviewed, and the pathogenesis of glioma was deeply understood, so as to find a better way for the diagnosis and treatment of glioma.
RESUMO
Glioma is one of the most common and invasive malignant tumors in the central nervous system. The Wnt-β-catenin signaling pathway is a classical Wnt pathway, which is involved in the occurrence and development of glioma and other tumors. Long non-coding RNA (LncRNA) is a functional RNA molecule without protein coding function, which plays a regulatory role in the occurrence and development of various tumors. Recent studies have shown that LncRNA and Wnt-β-catenin signaling pathways are jointly involved in glioma growth, invasion, migration and other processes, but the complex mechanism has not been thoroughly elaborated. In this paper, the influence of Wnt-β-catenin signaling pathway and its related LncRNA on glioma was reviewed, and the pathogenesis of glioma was deeply understood, so as to find a better way for the diagnosis and treatment of glioma.