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Trial and error disease regarding Asian home geckos using Enterococcus lacertideformus shows numerous ailment indication tracks and the in-vivo efficacy of prescription antibiotics.
t the biological processes regulated by hsa_circ_0000711 were mainly related to cell cycle regulation, so cell proliferation might be affected. The results of luciferase reporter gene and RT-qPCR assays showed that hsa_circ_0000711 directly bound to has-miR-103a-3p to serve as a molecular sponge. The results of CCK-8 and EdU staining assays revealed that the proliferation of hepatoma cells in hsa_circ_0000711 overexpression group was evidently enhanced. In addition, it was further found via flow cytometry that the apoptosis rate of cells was significantly raised in hsa_circ_0000711 low-expression group and dramatically declined in hsa_circ_0000711 overexpression group. CONCLUSIONS Overexpression of hsa_circ_0000711 promoted the proliferation and inhibited the apoptosis of hepatoma cells via targeting has-miR-103a-3p.OBJECTIVE The occurrence and progression of hepatocellular carcinoma (HCC) is a multi-step complex process and the exact molecular mechanisms remain to be elucidated. LncRNA NEAT1 is involved in tumorigenesis and progression. However, the role of LncRNA NEAT1 in HCC remains unclear. PATIENTS AND METHODS The tumor tissues and adjacent tissues of HCC patients were collected and LncRNA NEAT1 expression was detected by Real time PCR. The hepatoma cell line HepG2 was cultured and transfected with lnc RNA NEAT1 siRNA or lnc RNA NEAT1 plasmid followed by analysis of LncRNA NEAT1 expression, cell proliferation by MTT assay, as well as Caspase 3 activity. In addition, cell apoptosis and cell cycle were assessed by flow cytometry and cell invasion was measured by transwell chambers. The expression of EGFR, Bax and Bcl-2 was detected by Western blot. RESULTS LncRNA NEAT1 expression was significantly increased in HCC tissues compared with adjacent tissues (p less then 0.05). Compared with the siRNA group, transfection of lncRNA NEAT1 siRNA into HepG2 cells significantly inhibited cell proliferation, increased Caspase 3 activity and apoptosis, reduced cell invasion, as well as arrested cell cycle (p less then 0.05). Meanwhile, lncRNA NEAT1 siRNA also significantly decreased Bcl-2 and EGFR expression and increased Bax expression (p less then 0.05). selleck chemical Transfection of lncRNA NEAT1 plasmid in hepatoma cells HepG2 reversed the above changes, compared with vector group, the differences were statistically significant (p less then 0.05). CONCLUSIONS LncRNA NEAT1 expression is increased in liver cancer tissues. Down-regulation of LncRNA NEAT1 can inhibit EGFR expression and promote hepatoma cell apoptosis, inhibit cell cycle, thus inhibiting tumor proliferation and invasion.OBJECTIVE Recently, the role of long noncoding RNA (lncRNAs) in tumor progression has attracted much attention. The aim of this study was to investigate the role of lncRNA SNHG16 in the development of Wilms' tumor, and to explore the underlying mechanism. PATIENTS AND METHODS Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was used to detect SNHG16 expression in Wilms' tumor patients' tissues. Function assays, including wound healing assay, and transwell assay, were conducted to detect the changes of biological behaviors in Wilms' tumor cells due to gain or loss of SNHG16. Besides, the luciferase reporter gene assay was performed to explore the underlying mechanism. RESULTS The expression level of SNHG16 was significantly up-regulated in Wilms' tumor tissues when compared with adjacent tissues. Cell migration and invasion abilities were significantly repressed via down-regulation of SNHG16. However, opposite results were obtained after up-regulation of SNHG16 in vitro. After the down-regulation of SNHG16, the expression of miR-200a-3p increased significantly. However, the expression of miR-200a-3p was remarkably reduced via up-regulation of SNHG16 in vitro. Furthermore, SNHG16 acted as a competing endogenous RNA via sponging miR-200a-3p in Wilms' tumor. CONCLUSIONS SNHG16 induced the metastasis of Wilms' tumor via sponging miR-200a-3p. Our findings might provide a new prospect for the diagnosis and therapy of Wilms' tumor.OBJECTIVE Many studies showed that long non-coding RNAs (lncRNAs) may serve as prospective markers for patients with malignant cancers, including cervical cancer (CC). In this study, we mainly investigate the functions of lncRNA PTENP1 in the progression of human CC. MATERIALS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to detect expression levels of PTENP1, miR-19b and MTUS1 in CC tissues, the adjacent tissues and CC cell lines. The correlations between PTENP1 with miR-19b, miR-19b with MTUS1 and PTENP1 with MTUS1 were analyzed. Overall survival (OS) of patients was analyzed using Kaplan-Meier method. Proliferation capacity was measured by CCK-8 assay and the invasion ability in CC cell line was detected by transwell assay. Western blot (WB) assay was performed to measure protein levels of tissues and CC cell lines. Finally, Dual-Luciferase reporter assay was performed to prove the potential binding sites between PTENP1 and miR-19b, miR-19b and MTUS1. RESULTS We found inhibit cell proliferation and invasion via miR-19b/MTUS1 in CC patients, which uncovered the tumor-suppressive role of PTENP1 in CC and suggested that it might be a potential target for treating human CC.OBJECTIVE Over-expression of the epidermal growth factor receptor (EGFR) protein, along with gene amplification, is closely associated with recurrent cervical cancer and the disease's advanced stages. Additionally, it can have a direct impact on the disease's prognosis. The following are the members of the HER family (i) EGFR/HER1; (ii) HER2; (iii) HER3; and (iv) HER4. Figure 1 shows its signalling pathway. The synergy between the members facilitates immune escape by tumour cells, which can lead to tolerance to HER inhibitors. A broad HER inhibitor, a pan-HER inhibitor, can irreversibly inhibit a cell membrane's HER receptors to their ligands, thereby blocking downstream signal-transduction cascades, inhibiting tumour growth, adhesion, invasion, differentiation, and metastasis. As such, pan-HER inhibitors may be an area of interest in treating recurrent or late-stage cervical cancer. MATERIALS AND METHODS Through a review of HER-family receptors and their molecular mechanism, we can conclude that pan-HER inhibitors do indeed have a positive impact on therapy for recurrent or late-stage cervical cancer patients.
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