microRNA-141-3p fosters the growth, invasion, and tumorigenesis of cervical cancer cells by targeting FOXA2
Jia-Heng LiZhan ZhangMingze DuYichun GuanJianning YaoHaiyang YuBijun WangXingling WangSheling WuZhen Li
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Ectopic expression
Long non‑coding RNAs (lncRNAs) and microRNAs (miRs) have been reported to regulate disease progression in numerous types of disease, including retinoblastoma (Rb). Therefore, the present study aimed to investigate the effects of the lncRNA FEZ family zinc finger 1 antisense RNA 1 (FEZF1‑AS1) on Rb and to determine its possible mechanism of action. Reverse transcription‑quantitative PCR and western blot analysis were conducted to detect the gene or protein expression. Cell Counting Kit‑8, wound healing and transwell invasion assays were performed to estimate the capabilities of cell viability, invasion and migration. The potential association between FEZF1‑AS1 and miR‑1236‑3p in Y79 cells was measured via dual‑luciferase reporter assay. The results of the present study revealed that the levels of FEZF1‑AS1 were significantly upregulated in different Rb cell lines, with the most prominent upregulation observed in Y79 cells. In addition, the cell viability, invasive and migratory abilities, and the ability to undergo epithelial‑mesenchymal transition (EMT), were significantly inhibited following the transfection of short hairpin RNA (shRNA)‑FEZF1‑AS1 into Y79 cells. Further experimental validation confirmed that miR‑1236‑3p may be a direct target of FEZF1‑AS1. Notably, the miR‑1236‑3p inhibitor was discovered to reverse the inhibitory effects of shRNA‑FEZF1‑AS1 on cell viability, invasion, migration and EMT. In conclusion, the findings of the present study suggested that lncRNA‑FEZF1‑AS1 may promote the viability, migration, invasion and EMT of Rb cells by modulating miR‑1236‑3p.
Retinoblastoma
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This chapter contains sections titled: Introduction Gene Silencing—The Basic Parts List Mechanisms of Silencing Gene Silencing in Oomycetes: Tales from the Laboratory and Clues from Genomes Strategies for Application of Gene Silencing in Oomycetes Validation: Linking Gene Silencing to Phenotype Which Strategy? Stable versus Transient Gene Silencing Conclusions and Scope for Future Work Acknowledgments References
RNA-induced silencing complex
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Gene silencing is one of the important factors of transgene inactivation. The main mechanisms , including postion effects, transcriptional silencing and post transcriptional silencing was presented , the means of stabilizing gene expression in transgeneic plants was discussed.
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Intracellular siRNA release is a crucial step in efficient gene silencing mediated by cationic polymers. Here, we show an example of temperature change-induced intracellular siRNA release and silencing using a temperature-responsive polymer consisting of dendrimer, poly(N-isopropylacrylamide) and phenylboronic acid. The smart polymer can trigger the release of loaded siRNA in a controlled manner upon cooling the surrounding solution below its lower critical solution temperature. Gene silencing efficacy of the polymer was significantly increased by cool treatment after its cellular uptake. The polymer and the cool treatment cause minimal toxicity to the transfected cells. The results provide a facile and promising strategy to design stimuli-responsive polymers for efficient gene silencing.
Phenylboronic acid
Cationic polymerization
Smart polymer
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This study aimed to determine whether manipulation of the microRNA‑200 (miR‑200) family could influence colon adenocarcinoma cell behavior. The miR‑200 family has a significant role in tumor suppression and functions as an oncogene. In vitro studies on gain and loss of function with small interfering RNA demonstrated that the miR‑200 family could regulate RASSF2 expression. Knockdown of the miR‑200 family in the HT‑29 colon cancer cell line increased KRAS expression but decreased signaling in the MAPK/ERK signaling pathway through reduced ERK phosphorylation. Increased expression of the miR‑200 family in the CCD‑841 colon epithelium cell line increased KRAS expression and led to increased signaling in the MAPK/ERK signaling pathway but increased ERK phosphorylation. Functionally, knockdown of the miR‑200 family led to decreased cell proliferation in the HT‑29 cells; therefore, increased miR‑200 family expression could increase cell proliferation in the CCD‑841 cell line. The present study included a large paired miR array dataset (n=632), in which the miR‑200 family was significantly found to be increased in colon cancer when compared with normal adjacent colon epithelium. In a miR‑seq dataset (n=199), the study found that miR‑200 family expression was increased in localized colon cancer compared with metastatic disease. Decreased expression was associated with poorer overall survival. The miR‑200 family directly targeted RASSF2 and was inversely correlated with RASSF2 expression (n=199, all P<0.001). Despite the well‑defined role of the miR‑200 family in tumor suppression, the present findings demonstrated a novel function of the miR‑200 family in tumor proliferation.
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Ectopic expression
Expression (computer science)
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Zinc finger protein 24 (ZNF24) has been demonstrated to regulate proliferation, differentiation and migration as well as invasion in several types of cells. However, the molecular role and clinical effects of ZNF24 in prostate cancer (PCa) remain unclear. The present study revealed that ZNF24 expression is upregulated in PCa, and associated with tumor volume, Gleason score, pathological grade and metastasis. Wound healing and Transwell invasion assays revealed that ectopic ZNF24 expression facilitated cell migration and invasion through the Twist1-induced epithelial-to-mesenchymal transition (EMT) process. In addition, colony formation and Cell Counting Kit-8 assays were used to determine the regulatory effects of ZNF24 on proliferation. The results suggested that ZNF24 also promoted cell proliferation in PCa. ZNF24 acted as an oncogene and promoted migration, invasion and EMT of PCa cells via the regulation of Twist1.
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The analysis of oncogene expression may provide insights into the pathogenesis of small cell lung cancer (SCLC) and may help to predict clinical behavior. The expression of 8 oncogenes (c-myc, N-myc, L-myc, Ha-ras, Ki-ras, N-ras, erbB-2, v-sis) was evaluated in small cell lung cancer (SCLC) xenografts of tumor samples, recentlly transplanted, taken from 17 different patients. Eight of these 17 SCLC lines expressed the L-myc oncogene and 2 SCLC lines expressed the c-myc oncogene. One SCLC line (SCLC-63M) simultaneously expressed the L-myc and c-myc oncogenes. All SCLC lines examined had almost similar high RNA levels of the Ki-ras oncogene, while the expression of Ha- and N-ras oncogenes was not always observed. The N-myc and v-sis oncogenes were expressed in only one tumor and at a very weak level, and no transcript of the erbB-2 oncogene was observed in any of our 17 SCLC lines. These results indicate that oncogene expression in SCLC lines is heterogeneous, with the exception of the Ki-ras oncogene which is constantly overexpressed.
N-Myc
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The long non-coding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) has been identified as an oncogene in numerous diseases, and aberrant lncRNA PVT1 expression has been associated with the development of cancer. However, the underlying mechanism by which lncRNA PVT1 affects cell invasion in esophageal cancer has been not demonstrated. In the current study, the expression of lncRNA PVT1 was found to be increased in esophageal cancer specimens (n=77) by reverse transcription-quantitative polymerase chain reaction, and was correlated with tumor stage (P=0.009) and metastasis (P<0.001). In vitro, by using transwell assay, upregulation of lncRNA PVT1 promoted the invasion of TE-1 esophageal cancer cells; while downregulation of lncRNA PVT1 inhibited Eca-109 cell invasion. In addition, western blot analysis indicated that upregulation of lncRNA PVT1 may induce epithelial-to-mesenchymal transition (EMT) by regulating the expression levels of EMT markers (E-cadherin, N-cadherin and vimentin). In conclusion, lncRNA PVT1 is able to regulate the invasion of esophageal cancer cells by inducing EMT.
PVT1
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