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Utilizing a content database and knowledge blend approach to accelerate the procedure design development of higher shear damp granulation.
Knockdown of LINC00473 significantly inhibited cell growth, invasion, and migration of PANC-1 cells. LINC00473 activated cAMP and then promoted the phosphorylation of β-catenin to promote the progression of PC. Furthermore, high expression of LINC00473 and β-catenin remarkedly indicated poor prognosis of PC patients. Conclusions LINC00473 was upregulated in PC tissues and cells, indicating a poor prognosis and clinical pathological features of PC. It promoted PC progression via activating the cAMP/β-catenin axis, which provided a novel target for the prediction for PC diagnosis, biological therapy, and prognosis.Objective To study the influences of metformin on the proliferation and apoptosis of pancreatic cancer cells and its dose-effect relationship and crucial molecular mechanism. Materials and methods With human pancreatic cancer cell line PANC-1 as the study object, different concentrations of metformin were added for intervention. Then, the proliferation of PANC-1 cells was detected via methyl thiazolyl tetrazolium (MTT) assay to determine the dose-effect relationship of metformin in PANC-1 cell proliferation. PANC-1 cells were treated with metformin at three appropriate concentrations as Metformin treatment groups, and an equal amount of dimethyl sulfoxide (DMSO) was added in Control group. Flow cytometry was performed to detect PANC-1 cell cycle and apoptosis, and the apoptosis of PANC-1 cells was also evaluated via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Caspase-3 protein localization and expression in PANC-1 cells were detected using immunofluorescence assay. Besformin modulates the mTOR signaling pathway to reduce the proliferation of pancreatic cancer cell, but increase their apoptosis.Objective To uncover the potential influence of microRNA-203a-5p (miRNA-203a-5p) on the malignant progression of Wilms' tumor (WT). Patients and methods MiRNA-203a-5p levels in 49 paired WT and paracancerous tissues were determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Prognostic value of miRNA-203a-5p in WT was assessed by the Kaplan-Meier method. Pemigatinib chemical structure Correlation between miRNA-203a-5p level and clinical data of WT patients was analyzed. In G401 and SK-NEP-1 cells, in vitro functions of miRNA-203a-5p in regulating metastatic abilities were explored. The interaction between miRNA-203a-5p and JAG1, and their regulatory role in the malignant progression of WT were evaluated by Dual-Luciferase reporter gene assay and rescue experiments. Results MiRNA-203a-5p was downregulated in WT tissues than that of paracancerous ones. WT patients expressing low level of miRNA-203a-5p had higher risk of lymphatic metastasis and worse prognosis. Overexpression of miRNA-203a-5p attenuated migratory and invasive abilities in G401 cells. On the contrary, knockdown of miRNA-203a-5p yielded the opposite trends in SK-NEP-1 cells. JAG1 was verified to be the direct gene binding miRNA-203a-5p, which was negatively regulated by miRNA-203a-5p in WT cells. Rescue experiments finally uncovered that miRNA-203a-5p alleviated the malignant progression of WT via negatively regulating JAG1. Conclusions MiRNA-203a-5p is downregulated in WT and closely linked to lymphatic metastasis of WT patients. By negatively regulating JAG1, miRNA-203a-5p alleviates the malignant progression of WT.Objective Long non-coding RNA (lncRNA) has been verified to regulate several cancers, including bladder cancer (BC). Our study aimed to elucidate the expression, function, and mechanism of lncRNA BRE-AS1 in BC. Patients and methods Relative expression of lncRNA BRE-AS1 in 77 BC tissues and adjacent normal tissues was determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Expression of lncRNA BRE-AS1 in T24 and EJ cells was up-regulated using lentivirus transfection. Cell counting kit-8 (CCK-8) assay and colony formation assay were used to assess the proliferation of T24 and EJ cells influenced by lncRNA BRE-AS1. Also, the influence of lncRNA BRE-AS1 on cell apoptosis and cell cycle was measured using flow cytometry. Western blot was employed to explore the downstream molecules for lncRNA BRE-AS1 in BC. In vivo, xenograft formation experiment was established in nude mice to study the function of lncRNA BRE-AS1 in BC. Results LncRNA BRE-AS1 showed significantly decreased expression in BC tissues than the paired normal tissues. In vitro experiments demonstrated that over-expression of lncRNA BRE-AS1 inhibited cell proliferation but promoted cell apoptosis of EJ and T24 cells. STAT3 was determined as a target for lncRNA BRE-AS1. In vivo, up-regulation of lncRNA BRE-AS1 reduced cancer growth in nude mice bearing BC via repressing the phosphorylation of STAT3. Conclusions LncRNA BRE-AS1 was down-regulated in BC tissues. Over-expression of lncRNA BRE-AS1 inhibited BC cell proliferation in vitro and in vivo via repressing the phosphorylation of STAT3. This might provide a new sight for the understanding of BC progression and biotherapy.Objective The purpose of this study was to investigate the expression characteristics of circular RNA circ_0061140 in bladder cancer (BCa), and to further explore its effects on invasiveness and migration capacity of BCa cells, as well as its possible potential mechanism. Patients and methods Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression level of circ_0061140 in tumor tissue samples and paracancerous ones collected from 42 patients with BCa, and the interplay between circ_0061140 level and the clinical indicators, as well as the prognosis of BCa patients were analyzed. Meanwhile, qRT-PCR was also used to verify circ_0061140 expression in BCa cell lines. In addition, a circ_0061140 knockdown model was constructed using Lentiviral in BCa cell lines, including T24 and 253j, and the effect of circ_0061140 on BCa cell functions and its underlying mechanisms were explored using Cell Counting Kit-8 (CCK-8), transwell, and cell wound healing assays. Results qPCR reto proliferate and invade, suggesting that the two may regulate each other. Conclusions Circ_0061140 level was found remarkably elevated in BCa tissues, as well as in cell lines, which was closely relevant to the incidence of lymph node or distant metastasis of BCa patients. In addition, circ_0061140 may enhance the proliferation rate and invasion ability of BCa cells through the modulation of microRNA-1236.
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