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Meanwhile, we demonstrated that microRNA-486 (miR-486) was involved in PVT1-induced migration and invasion. We also uncovered that miR-486 was downregulated in osteosarcoma tissue specimens and cell lines. Functionally, we showed that upregulation of miR-486 reversed the facilitative effect of PVT1 on osteosarcoma cells migration and invasion, and vice versa. Ki20227 manufacturer Mechanically, we illustrated that PVT1 interacted with miR-486 in a reciprocal suppressed manner. Moreover, we found that miR-486 could target to PVT1 via Luciferase assay. Lastly, we proved that PVT1 promoted osteosarcoma cells migration and invasion through miR-486 sponging. CONCLUSIONS We demonstrated that PVT1, functioning as an oncogene, promotes osteosarcoma cells metastasis via miR-486 sponging. PVT1/miR-486 axis might be a novel target in the molecular treatment of osteosarcoma.OBJECTIVE To clarify the role of LINC00675 in affecting the progression of clear cell renal cell carcinoma (ccRCC) and its potential mechanism, thus providing effective hallmarks and therapeutic targets for the clinical treatment of ccRCC. MATERIALS AND METHODS Differentially expressed long non-coding RNAs (lncRNAs) in renal epithelial tissues and ccRCC tissues were searched by analyzing the dataset downloaded from The Cancer Genome Atlas (TCGA) and LINC00675 was selected. LINC00675 level in ccRCC cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Overexpression model of LINC00675 model in 786-O and 769-P cells was constructed by the transfection of pcDNA3.1(+)-LINC00675 (LV-LINC00675). Changes in proliferative, migratory, and invasive capacities of 786-O and 769-P cells overexpressing LINC00675 were assessed. At last, relative levels of β-catenin, Vimentin, and N-cadherin in ccRCC cells overexpressing LINC00675 were detected by qRT-PCR and Western blot. RESULTS LINC00675 was downregulated in ccRCC tissues and cell lines. Overexpression of LINC00675 attenuated proliferative, migratory, and invasive capacities of 786-O and 769-P cells. Downregulation in β-catenin after overexpression of LINC00675, while Vimentin and N-cadherin levels did not change. CONCLUSIONS LINC00675 is downregulated in ccRCC. Overexpression of LINC00675 attenuates ccRCC to proliferate, migrate, and invade by activating the Wnt/β-catenin pathway.OBJECTIVE Dysregulation of microRNA-370 (miR-370) is involved in a variety of cancers, but its roles in bladder cancer (BC) remain largely unexplored. Therefore, we designed this study to explore the role of miR-370 in BC. PATIENTS AND METHODS We took advantage of biochemical assays, including RT-qPCR, Western blot, CCK-8, flow cytometry, transwell, xenograft tumor formation, and immunohistochemistry (IHC) for research. RESULTS The expression of miR-370 was found to be downregulated during the development of BC, highly correlating with the malignant transformation of tumors. The overexpression of miR-370 led to enhanced apoptosis in BC cells, while inhibiting cell proliferation, migration, and invasion, effectively blocking cancer metastasis. Additionally, we identified SOX12, a known human oncogene, as a direct target of miR-370, showing that upregulation of SOX12 attenuated miR-370-mediated tumor suppression, promoted tumor growth, and epithelial-mesenchymal transition (EMT) in BC. CONCLUSIONS Taken together, these findings help to elucidate the roles of miR-370 as a tumor suppressor in BC, providing a potential target for diagnosis and treatment of BC.OBJECTIVE The aim of this study was to determine the expression profile and the underlying mechanism of the long intergenic non-protein coding RNA AL161431.1 in EC (endometrial carcinoma). MATERIALS AND METHODS In this study, the expression data for the lncRNA AL161431.1 in EC was downloaded from The Cancer Genome Atlas (TCGA) database and used to examine its expression profile. quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) and Western blot analysis were used to detect gene and protein expression, respectively. A subcellular fractionation assay was used to determine the location of AL161431.1. Cell Counting Kit-8 (CCK-8) and colony formation assays were used to evaluate cellular proliferation. Cell migration and wound healing assays were used to detect the effects on cell migration. RNA pull-down and Luciferase reporter assays were used to confirm the interaction between AL161431.1 and miR-1252-5p. RESULTS High expression levels of AL161431.1 were observed in EC patients, tissues, and cells. Loss-of-function experiments validated the carcinogenic role of AL161431.1. Based on the determined cytoplasmic location of AL161431.1, we investigated the ceRNA network and its relation to AL161431.1, miR-1252-5p, and MAPK (mitogen-activated protein kinase) signaling in EC. The molecular mechanism of the interaction between AL161431.1 and miR-1252-5p, and its effects on the MAPK signaling pathway was validated using rescue experiments in Ishikawa cells. CONCLUSIONS Our novel results indicate that AL161431.1 targets and binds to miR-1252-5p, resulting in the de-repression of MAPK signaling in EC cells. This highlights the potential for AL161431.1 to be targeted as a potent therapeutic strategy in the treatment of EC.OBJECTIVE Accumulating evidence determined that lncRNA plays important roles in the development and occurrence of cancers. Prostate cancer is the second most common type of cancer and one of the top five cancers for the cause of male death in the world. Therefore, this study was to explore the regulatory mechanism of lncRNA in chemoresistance of PC. MATERIALS AND METHODS qRT-PCR was used to detect the mRNA expression of FEZF1-AS1, miR-25-3p and ITGB8. Western blot was applied to measure the protein expression of ITGB8 E-cadherin, N-cadherin, Vimentin, LC3I, LC3II, ATG5 and Beclin-1. In addition, CCK-8 assay was used to assess cell proliferation of transfected cells. Luciferase reporter assay and RIP assay were used to determine the relationship among FEZF1-AS1, miR-25-3p and ITGB8. RESULTS In this study, the expression of FEZF1-AS1 and ITGB8 was upregulated, whereas the expression of miR-25-3p was downregulated in PC tumor tissues and PC/PTX cells. Luciferase reporter assay and RIP assay determined that miR-25-3p was a target of FEZF1-AS1 and ITGB8 was a target mRNA of miR-25-3p.