Parecoxib inhibits glioblastoma cell proliferation, migration and invasion by up-regulating miRNA-29c
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Glioblastoma (GBM) is one of the most lethal brain cancers worldwide, and there is an urgent need for development of novel therapeutic approaches. Parecoxib is a well-known cyclooxygenase-2 (COX-2) inhibitor, had already been developed for postoperative analgesia with high efficience and low adverse reaction. Recent study suggested that parecoxib potently enhances immunotherapeutic efficacy of GBM, but its effects on GBM growth, migration and invasion had never been studied before. In the present study, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and, BrdU (5-Bromo-2-deoxyUridine) incorporation assays were used to evaluate the cell proliferation of GBM cells. Wound-healing and Transwell assays were preformed to analyze GBM cell migration and invasion, respectively. The results suggested that parecoxib inhibits cell proliferation, migration and invasion of GBM cells in a dose-dependent manner. RT-qPCR (Quantitative Real-time PCR) analysis demonstrated that miRNA-29c can be significantly induced by parecoxib. Furthermore, our data suggested that miRNA-29c inhibitor can significantly attenuate parecoxib's effect on proliferation, migration and invasion of GBM. In conclusion, the present study suggested that parecoxib inhibits GBM cell proliferation, migration and invasion by up-regulating miRNA-29c.Keywords:
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Glioblastoma (GBM) is one of the most lethal brain cancers worldwide, and there is an urgent need for development of novel therapeutic approaches. Parecoxib is a well-known cyclooxygenase-2 (COX-2) inhibitor, had already been developed for postoperative analgesia with high efficience and low adverse reaction. Recent study suggested that parecoxib potently enhances immunotherapeutic efficacy of GBM, but its effects on GBM growth, migration and invasion had never been studied before. In the present study, MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and, BrdU (5-Bromo-2-deoxyUridine) incorporation assays were used to evaluate the cell proliferation of GBM cells. Wound-healing and Transwell assays were preformed to analyze GBM cell migration and invasion, respectively. The results suggested that parecoxib inhibits cell proliferation, migration and invasion of GBM cells in a dose-dependent manner. RT-qPCR (Quantitative Real-time PCR) analysis demonstrated that miRNA-29c can be significantly induced by parecoxib. Furthermore, our data suggested that miRNA-29c inhibitor can significantly attenuate parecoxib's effect on proliferation, migration and invasion of GBM. In conclusion, the present study suggested that parecoxib inhibits GBM cell proliferation, migration and invasion by up-regulating miRNA-29c.
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Competing Endogenous RNA
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Aberrant expression of microRNAs (miRNAs) has been implicated in cancer initiation and progression. In this study, we found that microRNA-34a (miR-34a) is significantly downregulated in glioblastoma multiforme (GBM) specimens compared with normal brain tissues. Growth curve and colony formation assays revealed that miR-34a suppresses proliferation of U373MG and SHG44 glioblastoma cells. Overexpression of miR-34a could induce apoptosis of glioblastoma cells. Also, we identified notch1 as a direct target gene of miR-34a. Knockdown of notch1 showed similar cellular functions as overexpression of miR-34a both in vitro and in vivo. Collectively, our findings show that miR-34a is downregulated in GBM cells and inhibits GBM growth by targeting notch1.
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The dysregulation of microRNA (miRNA) expression is closely related with tumorigenesis and tumor development in glioblastoma (GBM). In this study, we found that miRNA-598 (miR-598) expression was significantly downregulated in GBM tissues and cell lines. Restoring miR-598 expression inhibited cell proliferation and invasion in GBM. Moreover, we validated that metastasis associated in colon cancer-1 (MACC1) is a novel target of miR-598 in GBM. Restoring MACC1 expression reversed the inhibitory effects of miR-598 overexpression on GBM cells. In addition, miR-598 overexpression suppressed Met/AKT pathway activation in GBM. Our results provided compelling evidence that miR-598 serves tumor-suppressive roles in GBM and that its antioncogenic effects are mediated chiefly through the direct suppression of MACC1 expression and regulation of the Met/AKT signaling pathway. Therefore, miR-598 is a potential target in the treatment of GBM.
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microRNA‑145 (miR‑145) has been reported to be frequently downregulated in various types of cancer, including renal, prostate, bladder, lung and colon cancer, as well as B‑cell malignancies. The present study examined the effects of miR‑145 on the cell proliferation, migration and invasion of renal cell carcinoma (RCC). Following transfection of miR‑145, an MTT, cell migration, cell invasion and luciferase assays, and western blot analysis were conducted in RCC cell lines. The present study demonstrated that miR‑145 inhibited cell proliferation, migration and invasion in 786‑O and A498 cells. The present study also demonstrated for the first time, to the best of our knowledge, that miR‑145 may directly target matrix metallopeptidase‑11 (MMP‑11) in RCC. miR‑145 was demonstrated to suppress cell proliferation, migration and invasion by targeting MMP‑11 in RCC cell lines. These results suggested that it may be investigated as a predictive marker for the early detection of tumor metastasis and for targeting therapeutic drugs to inhibit the invasion of RCC.
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MicroRNAs are noncoding RNAs of 21 to 23 nucleotides in length that play important roles in almost all biological pathways. The roles of microRNA-299-3p in the development and progression of oral squamous cell carcinoma remain unclear. Expression level of microRNA-299-3p in oral squamous cell carcinoma cell lines was analyzed. Then, the effects of microRNA-299-3p on oral squamous cell carcinoma cell proliferation and migration were investigated. Moreover, bioinformation algorithm and Western blot were conducted to explore whether forkhead box P4 was a direct target of miR-299-3p. We showed that microRNA-299-3p expression was significantly reduced in oral squamous cell carcinoma cell lines. Next, overexpression of microRNA-299-3p was found to inhibit oral squamous cell carcinoma cell proliferation and migration but promote apoptosis. In addition, forkhead box P4 was identified as a functional target of microRNA-299-3p. Our results provide a new perspective for the mechanisms underlying the progression of oral squamous cell carcinoma and a novel target for the treatment of oral squamous cell carcinoma.
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The functional integrity of the intestinal epithelial barrier relies on tight coordination of cell proliferation and migration, with failure to regulate these processes resulting in disease. It is not known whether cell proliferation is sufficient to drive epithelial cell migration during homoeostatic turnover of the epithelium. Nor is it known precisely how villus cell migration is affected when proliferation is perturbed. Some reports suggest that proliferation and migration may not be related while other studies support a direct relationship. We used established cell-tracking methods based on thymine analog cell labeling and developed tailored mathematical models to quantify cell proliferation and migration under normal conditions and when proliferation is reduced and when it is temporarily halted. We found that epithelial cell migration velocities along the villi are coupled to cell proliferation rates within the crypts in all conditions. Furthermore, halting and resuming proliferation results in the synchronized response of cell migration on the villi. We conclude that cell proliferation within the crypt is the primary force that drives cell migration along the villus. This methodology can be applied to interrogate intestinal epithelial dynamics and characterize situations in which processes involved in cell turnover become uncoupled, including pharmacological treatments and disease models.—Parker, A., Maclaren, O. J., Fletcher, A. G., Muraro, D., Kreuzaler, P. A., Byrne, H. M., Maini, P. K., Watson, A. J. M., Pin, C. Cell proliferation within small intestinal crypts is the principal driving force for cell migration on villi. FASEB J. 31, 636–649 (2017). www.fasebj.org
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A growing body of research suggests that microRNAs (miRNAs) may play a key part in the progression of various cancers, including lung adenocarcinoma (LUAD). However, the expression and mechanism of miR-938 (microRNA-938) in LUAD have not been defined. Compared with adjacent tissues, the level of miR-938 was up-regulated in LUAD tissues. miR-938 expression was significantly associated with tumor size. In vitro assays indicated that miR-938 expression was also increased in the LUAD cell lines. Overexpression of miR-938 promoted LUAD cell proliferation, whereas down-regulation of miR-938 had the opposite effect. We identified RNA-binding protein 5 (RBM5) as a potential target gene of miR-938 in LUAD. Expression of RBM5 was down-regulated in LUAD tumor tissues and negatively correlated with expression of miR-938. Up-regulation of RBM5 reversed cell proliferation by inhibition of miR-938 expression in LUAD cells. These results showed that miR-938 may act as an oncogenic miRNA by targeting RBM5 in LUAD, indicating that miR-938 could be used as a potential therapeutic target for LUAD patients.
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MicroRNA (miRNA-221) has been reported to be a regulator of cell proliferation. Here we intended to investigate the role of miRNA-221 in regulating the growth of human non-small cell lung cancer cell line H460. H460 cells were transfected with miRNA-221 mimics/inhibitors or their respective negative controls. Real-time quantitative PCRs (qRT-PCRs) were used to confirm the effects of miRNA-221 mimics and inhibitors in H460 cells while Cell Counting Kit 8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) assay were used to access the cell viability and proliferation. P27 and P57, as putative targets of miRNA-221, were determined by qRT-PCRs in H460 cells. We found that overexpression of miRNA-221 led to increased proliferative rate and cell viability in H460 cells while down-regulation of miRNA-221 decreased those effects. P27 but not P57 was identified as a potential target gene of miRNA-221 in H460 as P27 was negatively regulated by miRNA-221 in the protein level. In conclusion, this study suggests that miRNA-221 controls human non-small cell lung cancer cell H460 growth potentially by targeting P57. Inhibition of miRNA-221 represents a novel potential treatment for human non-small cell lung cancer.
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