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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. 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. selleck chemicals 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.Objective The importance of circular RNAs in malignant tumors causes more attention in researchers. link2 Circular RNA_LARP4 is identified as a tumor suppressor in gastric cancer, but the role of circular RNA_LARP4 in prostate cancer (PCa) remains unclear. Our work aims to uncover whether and how circular RNA_LARP4 functions in the PCa development. Patients and methods Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) was utilized to determine the level of circular RNA_LARP4 in PCa tissues and cell lines. The patients' prognosis was analyzed. Circular RNA_LARP4 lentivirus was constructed for transfection of PCa cells. Cell migrated and invaded ability was detected through wound healing assay and transwell assay. Western blot assay was performed to analyze the protein level of FOXO3A. Results The low circular RNA_LARP4 expression was associated with poor prognosis of PCa patients. The circular RNA_LARP4 was lowly expressed in PCa tissues compared with adjacent samples. The expression of circular RNA_LARP4 was downregulated in PCa cell lines. The cell migrated and invaded ability of PCa cells was inhibited after circular RNA_LARP4 was overexpressed. Furthermore, FOXO3A expression was increased via the overexpression of circular RNA_LARP4. Conclusions Circular RNA_LARP4 could suppress cell migration and invasion of PCa by upregulating FOXO3A.Objective Ovarian carcinoma (OC) is one prevalent fatal malignancy in gynecology. Currently, there is an imperative need to better investigate the pathogenesis of OC. Accumulating evidence has indicated that microRNAs (miRNAs) play pivotal roles in OC occurrence and development. In this study, we mainly investigated the potential roles of miR-18a in OC progression. Patients and methods We first examined miR-18a expressions in OC tissue samples and cell lines using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, OC patients involved in current study were assigned into two groups based on the mean miR-18a expression level. Kaplan-Meier analysis was carried out to assess the overall survival rate of miR-18a in OC patients. Next, we investigated whether miR-18a could regulate OC cell proliferation abilities by using MTT (3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide) assays. Next, transwell assay was used to detect the effects of miR-18a on cell invasion and migration. We fs an effective diagnostic and therapeutic biomarker for OC.Objective The purpose of this study was to investigate circRNA_MYLK level in ovarian cancer (OC), and to further investigate whether it could promote the malignant progression of OC via regulating microRNA-652. Patients and methods quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine circRNA_MYLK level in 46 tumor tissue specimens and paracancerous normal ones collected from OC patients, and the interplay between circRNA_MYLK expression and clinical indicators of OC and patient prognosis was analyzed. Meanwhile, qPCR was also used to further verify circRNA_MYLK level in OC cell lines. In addition, circRNA_MYLK knockdown model was constructed using lentivirus in OC cell lines including A2780 and CAOV3, and the impacts of circRNA_MYLK on the biological functions of OC cells was evaluated using Cell Counting Kit-8 (CCK-8) and cloning experiments. Finally, Luciferase reporting assay and recovery experiment were performed to investigate the regulatory interplay between circRNA_MYLK aote the malignant progression of OC via regulating microRNA-652, and its expression was remarkably associated with pathological staging and poor prognosis in patients with OC.Objective To explore possible mechanism of ERBB2 gene expression silencing mediating mitogen-activated protein kinase 1/mitogen-activated protein kinase 3 (MAPK1/MAPK3) signaling pathway on proliferation, migration, and invasion of ovarian cancer cells. Patients and methods A total of 240 cancer specimens were collected in patients with epithelial ovarian cancer intraoperatively in our hospital from January 2015 to January 2018. Expressions of ERBB2, MAPK1, and MAPK3 in tissues were detected by immunohistochemistry. Following the culture of ovarian cancer cell lines, target cell line with high expression of ERBB2 was screened by qRT-PCR. Cell grouping was performed with four groups after transfection, including Blank group, negative control (NC) group, ERBB2 shRNA group, and ERBB2 overexpression group (shorted as ERBB2 group). The expression levels of ERBB2, MAPK1, MAPK3, vascular endothelial growth factor (VEGF), metalloproteases-2 (MMP-2), and tissue inhibitor of metalloproteases-2 (TIMP-2) were detected bywing statistically significant differences (All p less then 0.05). link3 By contrast, the expression levels of ERBB2, MAPK1, MAPK3, VEGF, and MMP-2 increased remarkably in ERBB2 group, while TIMP-2 decreased significantly, and cell proliferation, invasion, and migration ability increased evidently after transfection, with statistically significant differences (All p less then 0.05). Conclusions Silencing ERBB2 gene expression may inhibit the activation of MAPK1/MAPK3 signaling pathway and thus suppress the proliferation, invasion, and migration of ovarian cancer cells. Overexpression of ERBB2 gene can reverse those trends, which in turn support the role of ERBB2 gene expression silencing in molecular targeted therapy of ovarian cancer.
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