PLK1 was confirmed to be the target gene of miRNA-875-3p. PLK1 was upregulated in CRC tissues and cell lines, which was negatively regulated by miRNA-875-3p. MiRNA-875-3p alleviated the malignant progression of CRC via negatively regulating PLK1. CONCLUSIONS MiRNA-875-3p is downregulated in CRC, which is closely related to distant metastasis and poor prognosis of CRC patients. MiRNA-875-3p alleviates the progression of CRC through targeting and downregulating PLK1.OBJECTIVE The aim of this study was to investigate the potential effects of microRNA-135b-5p (miR-135b) on the development of malignant melanoma (MM) and the relevant mechanism.  https://www.selleckchem.com/products/liraglutide.html  PATIENTS AND METHODS The expression level of miR-135b in MM tissues and cells was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Online prediction software and luciferase reporter assays were used to predict and verify the possible target of miR-135b, respectively. Furthermore, the effects of the miR-135b on MM A375 cells were determined by Western blotting, MTT, and transwell assays. RESULTS MiR-135b was significantly down-regulated in MM. RING-box protein 1 (RBX1) was verified as a direct target of miR-135b. Subsequent experiments showed that down-regulation of RBX1 resulted from miR-135b up-regulation could significantly inhibit the proliferation, invasion, and migration abilities of MM cells. CONCLUSIONS MiR-135b inhibited the progression of MM by targeting RBX1. Our findings revealed that miR-135b/RBX1 might be a potential therapeutic target for the treatment of MM.OBJECTIVE Melanoma is one of the most ordinary malignant tumors. Recent studies have revealed that long noncoding RNAs (lncRNAs) play an important role in the progression of tumorigenesis. This work aims to identify how lncRNA NEAT1 functions in the progression of melanoma. PATIENTS AND METHODS NEAT1 expression of both melanoma patients' tissue samples and cell lines was detected by Real Time-quantitative Polymerase Chain Reaction (RT-qPCR). Moreover, the function of NEAT1 was identified by performing the proliferation and transwell assay in vitro. Besides, the underlying mechanism was explored through the Luciferase assay and RNA immunoprecipitation (RIP) assay. In addition, tumor formation and metastasis assays were also conducted in vivo. RESULTS In this research, NEAT1 expression was significantly higher in melanoma tissues compared with that in skin tissues with the melanocytic nevus. Cell proliferation and invasion of melanoma were inhibited after the knockdown of NEAT1 in vitro. Moreover, the results of further experiments revealed that microRNA-224-5p (miR-224-5p) was upregulated via the knockdown of NEAT1 and was also a direct target of NEAT1 in melanoma. Furthermore, tumor formation and metastasis of melanoma were inhibited via the knockdown of NEAT1 in nude mice. CONCLUSIONS Our study suggests that NEAT1 enhances melanoma cell proliferation and metastasis via sponging miR-224-5p in vitro and in vivo.OBJECTIVE The aim of this study was to investigate whether microRNA-625-3p participated in the malignant progression of gastric cancer and inhibited GCa metastasis by regulating EZH2 (Enhancer of zeste homolog 2). PATIENTS AND METHODS Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine the expression of microRNA-625-3p in 36 pairs of GCa tissues and para-cancerous tissues. The interplay between microRNA-625-3p level and clinical indexes or prognosis of GCa patients was analyzed. MicroRNA-625-3p mimics and inhibitors, as well as their negative controls, were transfected into GCa cell lines to establish microRNA-625-3p overexpression and down-regulation models in vitro, respectively. QRT-PCR was applied to further verify the transfection efficiency. Cell counting kit-8 (CCK-8), colony formation, and transwell assays were performed to analyze the impact of microRNA-625-3p on the proliferative and invasiveness abilities of GCa AGS and SGC-7901 cells. Finally, the regulatory mechaniell reverse experiment showed that EZH2 could offset the influence of microRNA-625-3p on the proliferation and metastasis GCa cells, thereby affecting the malignant progression of GCa. CONCLUSIONS MicroRNA-625-3p was remarkably correlated with lymph node or distant metastasis and poor prognosis of GCa patients. In addition, microRNA-625-3p might inhibit the malignant progression of GCa via modulating EZH2.OBJECTIVE Gastric cancer (GC) is one of the most common cancers in the world, with a high incidence and a poor prognosis. A large number of lncRNAs have been demonstrated to play multiple important roles in cancer development and progression. LncRNA is usually used as ceRNA and forms a regulatory network with miRNA in gastric cancer. However, the function and regulatory network of lncRNA in gastric cancer have not been fully elucidated. MATERIALS AND METHODS The qRT-PCR assay was used to detect DCST1-AS1 and miR-605-3p expression. Western blot was applied to measure the protein expression of CDK4, cyclin D1, MMP-2, MMP-9, cleaved caspase 3, Bcl-2, Bax and β-actin. MTT assay and flow cytometry were performed to assess cell proliferation and apoptosis, respectively. Transwell migration and invasion assay were used to determine cell migration capacity and invasion ability. Luciferase reporter assay was applied to determine the relationship of DCST-AS1 and miR-605-3p in GC. RESULTS In this study, we found that DCST1-AS1 was highly expressed while miR-605-3p was low expressed in GC tissues and cells. Moreover, DCST1-AS1 expression negatively regulated miR-605-3p expression in GC. Functionally test demonstrated that knockdown of DCST1 inhibited cell proliferation, migration and invasion as well as promoted cell apoptosis in GC cells. Interestingly, miR-605-3p has been verified to be a target miRNA of DCST1-AS1 with luciferase reporter assay. More than that, the reverse experiment determined that the inhibition of miR-605-3p could alleviate the suppressive effects of low DCST1-AS1 expression on cell growth in GC. CONCLUSIONS We proved the regulatory network of lncRNA DCST1-AS1 for the first time, and also explored and found that lncRNA DCST1-AS1 regulated cell proliferation, migration, invasion and apoptosis by regulation of miR-605-3p, providing a new therapeutic target for gastric cancer treatment.