The aim of this study was to analyze the biological effects of circ-0079593 and its potential mechanism in the progression of melanoma. Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was carried out to detect circ-0079593 expression in melanoma tissue samples and cell lines, and the relationship between circ-0079593 expression and prognosis of patients with melanoma was analyzed based on collected clinical information. Then, the melanoma cell line stably overexpressing circ-0079593 was constructed using lentiviral stable transfection technique, and then, Cell Counting Kit-8 (CCK-8) and transwell assays were carried out to detect the proliferation rate, migration, as well as invasion abilities of melanoma cells, respectively. In addition, the potential binding targets of circ-0079593 were searched through bioinformatics analysis, and the results were verified by Dual-Luciferase assay. It was found that, in comparison with the normal control group, circ-0079593 showed a significantly high exprmelanoma, circ-0079593 may serve as a cancer-promoting gene to accelerate the rates of cell proliferation and migration, which may exert its effects by elevating EGFR expression by binding to microRNA-433. Nasopharyngeal carcinoma (NPC) is the commonest malignant tumor. In this article, we aimed to examine the molecular role of lncRNA HEIH in the progression of NPC. We assessed the expression of HEIH, miR-193a-5p and CDK8 in NPC tissues and cells by real-time PCR. The cell proliferation, invasion and migration of SUNE-1 cells were examined by CCK-8 and transwell assay. Western blot assay was adopted to measure the protein expression level of CDK8. Dual-Luciferase reporter assay was adopted to evaluate the correlation between HEIH, miR-193a-5p and CDK8. We discovered that HEIH was high expressed and miR-193a-5p was reduced in both NPC tissues and cells. The upregulation of HEIH facilitated cell proliferation, migration and invasion of SUNE-1 cells. In addition, overexpression of miR-193a-5p restrained cell progression of SUNE-1 cells. Moreover, HEIH was proved to be a molecular sponge of miR-193a-5p in NPC. Besides that, CDK8 was found to be a direct target gene of miR-193a-5p in NPC. Furthermore, CDK8 knockdown suppressed cell progression of SUNE-1 cells. Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8. Our data demonstrated that HEIH overexpression promoted cell progression by sponging miR-193a-5p and upregulating CDK8. Currently, we aimed to illustrate the role of lncRNA differentiation antagonizing non-protein coding RNA (DANCR) and erb-b2 receptor tyrosine kinase 2 (ErbB2) in non-small cell lung cancer (NSCLC). Expression of DANCR, microRNA-1225-3p (miR-1225-3p) and ErbB2 mRNA was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) assays. The clinical value of DANCR was checked by a ROC curve analysis, a Kaplan-Meier analysis and a Pearson Chi-Square test. Transwell chamber assays were performed to determine the migration and invasion ability changes of SPCA1 and A549 cells. The protein expression of ErbB2 was tested by Western blot assays. https://www.selleckchem.com/products/mitosox-red.html The targeted binding effect between miR-1225-3p and DANCR or ErbB2 was confirmed by a Dual-Luciferase reporter assay and an RNA pull-down assay, respectively. In the current study, it was found that DANCR was upregulated and correlated with poor prognosis in patients with NSCLC. DANCR promoted NSCLC cells migration and invasion via upregulation of ErbB2. DANCR regulated ErbB2 at posttranscriptional level. Mechanically, it was illustrated that miR-1225-3p negatively regulated ErbbB2 and it-mediated migration and invasion via directly targeting in NSCLC cells. Meanwhile, it was showed that DANCR interacted with miR-1225-3p in a reciprocal suppression manner. Even further, through a RIP assay and a luciferase assay, we showed that DANCR interacted with miR-1225-3p through a microRNA response element (MRE-1225-3p) via directly binding. Finally, it was demonstrated that DANCR served as a miR-1225-3p sponge to promote ErbB2 expression and to facilitate ErbB2-mediated migration and invasion in NSCLC cells. In the current study, it was illustrated that DNACR promoted ErbB2-mediated migration and invasion via working as a ceRNA of miR-1225-3p in NSCLC cells. In the current study, it was illustrated that DNACR promoted ErbB2-mediated migration and invasion via working as a ceRNA of miR-1225-3p in NSCLC cells. To illustrate the role of LINC00641 in inducing the malignant progression of colorectal cancer (CRC) through the miRNA-424-5p/PLSCR4 feedback loop. LINC00641 levels in paired CRC and non-tumoral tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic potential in CRC was assessed by Kaplan-Meier method. Changes in proliferative and migratory abilities of HCT116 and SW620 cells transfected with si-LINC00641 were evaluated by 5-Ethynyl-2'- deoxyuridine (EdU), cell counting kit-8 (CCK-8) and transwell assay. The feedback loop LINC00641/miRNA-424-5p/PLSCR4 was identified through Dual-Luciferase reporter assay and its involvement in CRC progression was finally explored by rescue experiments. LINC00641 was upregulated in CRC tissues, which was an unfavorable factor to the overall survival of CRC. Proliferative and migratory abilities of HCT116 and SW620 cells were inhibited by knockdown of LINC00641. LINC00641 could competitively bind miRNA-424-5p, thereby abolishing its inhibitory effect on PLSCR4 expression. Knockdown of PLSCR4 could inhibit proliferative and migratory abilities of HCT116 and SW620 cells. LINC00641 stimulates proliferative and migratory abilities of CRC through the miRNA-424-5p/PLSCR4 feedback loop. LINC00641 stimulates proliferative and migratory abilities of CRC through the miRNA-424-5p/PLSCR4 feedback loop. In many cancers, long non-coding RNAs (lncRNA) are largely involved; they can regulate cell proliferation, migration, and invasion. However, the research of lncRNA regulation on pancreatic ductal adenocarcinoma is vacant. The aim of this article was to lucubrate the specific role of lncRNA LUCAT1 in regulating the progression of pancreatic cancer. Pancreatic cancer and adjacent tissues were collected, and the expression of LUCAT1, one potential involved LucRNA, was measured using real-time qPCR (RT-qPCR). Different pathological types of pancreatic cancer cell lines were cultured, and the expression difference of LncRNA LUCAT1 was detected by RT-qPCR, and two cell lines were selected for downstream experiments. si-RNA was used to knockdown the expression of LUCAT1, comparing the difference in expression of LUCAT1, characterizing cell proliferation by MTT and BrdU staining, detecting apoptosis, and cell cycle changes by flow cytometry. Meanwhile, Western blotting was used for the detection of cyclin expression and thus investigate two important associated signaling pathways.