000). By utilizing univariate and multivariate Cox proportional hazard analyses, we found that low IL-10 level in plasma was significantly associated with improved overall survival (OS) of mCRC patients treated with irinotecan-containing regimen-with optimal cutoff value of 5.525pg/mL, respectively (p =0.002). In addition, the low IL-10 expression level in tumor tissue was significantly associated with the improved OS for the irinotecan-containing regimen (p = 0.023). Our study demonstrated that IL-10 could act as a prognostic biomarker for mCRC patients undergoing irinotecan-containing chemotherapy. Our study demonstrated that IL-10 could act as a prognostic biomarker for mCRC patients undergoing irinotecan-containing chemotherapy. Osteosarcoma (OS) is one of the most common malignant bone tumors with a poor overall prognosis. MiR-1224-5p plays an important role in cancer, but its function and mechanism in OS have not been studied. The expression of miR-1224-5p and PLK1 was detected by qRT-PCR in OS cells, adjacent tissues, and cell lines. Dual-luciferase reporter gene assay was used to verify the interaction between miR-1224-5p and PLK1. The expression of miR-1224-5p and PLK1 was intervened by transfection with miR-1224-5p mimic, NC mimic, pc-NC and PLK1, respectively. MTT, colony formation assay, Transwell and flow cytometry were used to observe the cell proliferation, invasion and apoptosis. Western blot was used to detect the expression levels of PLK1, PI3K/AKT/mTOR signaling pathway-related proteins, autophagy-related proteins, and epithelial-mesenchymal transition (EMT)-related proteins in the cells. We found that miR-1224-5p was down-regulated and PLK1 expression was up-regulated in OS tissues and cells. On the other hand, it is further confirmed that PLK1 was a target gene of miR-1224-5p. Overexpression of miR-1224-5p inhibited the proliferation, invasion while promoted the apoptosis of OS cells, whereas overexpression of PLK1 promoted the proliferation, invasion and inhibited the apoptosis of OS cells. In the miR-1224-5p group (overexpression of miR-1224-5p), PI3K, AKT, and mTOR protein phosphorylation levels were significantly reduced, while autophagic activity was significantly activated, and the degree of EMT was significantly reduced. But the results in the PLK1 group (overexpression of PLK1) were the opposite. In addition, overexpression of miR-1224-5p reversed the effect of PLK1 upregulation on OS cells. MiR-1224-5p targets PLK1 to inhibit PI3K/AKT/mTOR signaling pathway, thus mediating the proliferation, invasion, apoptosis, autophagy and EMT in OS cells. MiR-1224-5p targets PLK1 to inhibit PI3K/AKT/mTOR signaling pathway, thus mediating the proliferation, invasion, apoptosis, autophagy and EMT in OS cells. Cervical cancer (CC) is the second serious health threat in women worldwide. LncRNA ( antisense RNA 1) has been observed to abnormally express in human cancers. However, the expression pattern, clinical significance and molecular mechanism of ZFAS1 have not been thoroughly studied in CC. qRT-PCR was performed to examine the differential expression of ZFAS1 in CC tissues and adjacent normal cervical tissues. https://www.selleckchem.com/CDK.html Gain- and loss-of-function experiments were constructed to test the functional role of ZFAS1 in CC by CCK-8, colony formation, transwell and xenograft models assays. Luciferase reporter, RNA immunoprecipitation (RIP), methylated RNA immunoprecipitation (MeRIP), RNA pull-down assays were used to reveal the underlying mechanisms. We found that ZFAS1 was significantly upregulated in CC tissues. Elevation of ZFAS1 correlated with advanced FIGO stage, lymph node and distant metastasis, and also indicated poor overall survival in patients with CC. Functional experiments demonstrated that ZFAS1 promoted CC cell proliferation, migration and invasion in vitro, and facilitated tumor growth and metastasis in vivo. Mechanistic investigation revealed that ZAFS1 sequestered miR-647, and this RNA-RNA interaction is regulated by METLL3-mediated m A modification. Our findings elucidate the functional roles of ZFAS1 and its m A modification in CC cells and indicate that ZFAS1 may be a promising target for CC treatment. Our findings elucidate the functional roles of ZFAS1 and its m6A modification in CC cells and indicate that ZFAS1 may be a promising target for CC treatment. Increasing evidences suggest that mitochondrial calcium uniporter (MCU), a selective channel responsible for mitochondrial Ca uptake, is involved in the progression of several cancers. In this study, we aimed to observe the clinical implications and biological functions of MCU in gastric cancer. The expression of MCU in 90 pairs of gastric cancer tissues and adjacent normal tissues was examined using immunohistochemistry and correlation between MCU expression and clinical features was analyzed. After construction of stable MCU knockdown or overexpression gastric cancer cells, mitochondrial membrane potential (MMP), wound healing and transwell assays were performed to examine MMP levels, migration and invasion. Subcutaneous xenograft tumors induced by gastric cancer cells transfected with MCU siRNAs or controls were constructed. Immunofluorescence was used to detect CD34 expression. Western blot was used to detect the expression of hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor er, which could become a potential therapeutic marker for gastric cancer. Our findings suggested that highly expressed MCU could promote migration, invasion, angiogenesis and growth of gastric cancer, which could become a potential therapeutic marker for gastric cancer. Pancreatic carcinoma cells exhibit a pronounced tendency to invade along and through intra and extrapancreatic nerves, even during the early stages of the disease, a phenomenon called perineural invasion (PNI). Thus, we sought to determine the effects of the simultaneous expression of soluble forms of GAS1 and PTEN (tGAS1 and PTEN-L) inhibiting tumor growth and invasiveness. We employed a lentiviral system to simultaneously express tGAS1 and PTEN-L; in order to determine the effects of the treatments, cell viability and apoptosis as well as the expression of the transgenes by ELISA and intracellular signaling as ascertained by the activation of AKT and ERK1/2 were measured; cell invasiveness was determined using a Boyden chamber assay; and the effects of the treatment were measured in vivo in a mouse model. In the present work, we show that the combined treatment with tGAS1 and PTEN-L inhibits the growth of pancreatic cancer cells, by reducing the activities of both AKT and ERK 1/2, decreases cell invasiveness, and restrains tumor growth in a mouse model.