Purpose Osteosarcoma is rare but fatal type of human malignancy. The high metastasis rate, late diagnosis, emergence of drug resistance against drugs such as doxorubicin, and the lack of therapeutic targets obstructs the treatment of osteosarcoma. The present investigation explores the anticancer properties of Fisetin against human osteosarcoma cells. Methods The cell viability was determined by WST-1 assay. DAPI and Annexin V/propidium iodide (PI) assays were used for detection of apoptosis. Flow cytometry was used for the determination of osteosarcoma MG-63 cell distribution. Wound healing and transwell assays were used for cell migration and invasion. Western blotting was used for protein expression analysis. Results The results showed that Fisetin inhibits the growth of the MG-63 cells in a dose-dependent manner. Fisetin showed an IC50 of 18 µM against the MG-63 cells. The growth inhibitory effects of Fisetin were mainly due to induction of apoptosis which was accompanied by enhancement of the capsase-3 and Bax and depletion of Bcl-2 expression. Fisetin treatment increased reactive oxygen species (ROS) from 100 in untreated to 220% at 36 µM and decreased mitochondrial membrane potential (MMP) levels from 100 in untreated to 21% at 36 µM. Fisetin also induced G2/M cell cycle arrest of the MG-63 cells and suppressed the expression of cyclin-B1. The wound healing and the transwell assay showed that Fisetin suppressed the migration and invasion of the MG-63 cells. Conclusion Taken together, Fisetin may find use as lead molecule in the osteosarcoma therapeutic development programmes.Purpose The purpose of this study was to investigate the expression of microRNA (miRNA)-301a in osteosarcoma (OS) and its relationship with clinicopathological parameters and prognosis of patients with OS, and to further explore how it accelerates the progression of OS via modulating downstream target genes. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was used to examine the expression of miRNA-301a in 39 OS tumor tissue samples and adjacent ones, and the interplay between miRNA-301a and clinical indicators. The prognosis of patients with OS was analyzed. S961 In addition, miRNA-301a overexpression vector was constructed to analyze the effect of miRNA-301a on the function of OS cells by cell counting kit-8 (CCK-8), transwell and cell wound healing assays. Finally, the potential mechanism was also investigated using luciferase reporter gene assay and cell recovery experiment. Results qRT-PCR results revealed that miRNA-301a level in OS tumor tissue specimen was remarkably lower than that in adjacent tissue. Compared with patients with high expression of miRNA-301a, patients with low expression had a higher incidence of distant metastasis and lower overall survival. Compared with the negative control group (miR-NC group), cell proliferation and metastasis ability were remarkably decreased in the miRNA-301a mimics group. In addition, DEC2 expression was found remarkably elevated in OS cell lines and negatively correlated with miRNA-301a level. At the same time, cell recovery experiment demonstrated that there existed a mutual regulation between miRNA-301a and DEC2, the two of which could together promote the malignant progression of OS. Conclusions MiRNA-301a level was remarkably reduced both in OS tissues and cell line samples, and was confirmed to be associated with distant metastasis and poor prognosis of patients with OS. In addition, miRNA-301a was found to be able to inhibit malignant progression of OS through regulating DEC2.Purpose To detect the expression level of long non-coding ribonucleic acid 01555 (linc01555) in gastric cancer (GC) tissues and cells, and its effects on the biological functions of GC cells. Methods The relative expression of linc01555 in 61 cases of GC and para-carcinoma tissues and GC cells was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). GC cells were divided into experimental group (si-linc01555) and control group (si-NC), and the interference efficiency was detected through qRT-PCR. The effects of interference in linc01555 expression on GC cell proliferation, colony formation ability, migration and invasion were determined using cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay and Transwell assay. Moreover, the expressions of molecular markers in the downstream Notch pathway were detected using western blotting. Results The results of qRT-PCR showed that the expression of linc01555 was upregulated in GC tissues and cells. The results of CCK-8 assay revealed that the proliferative activity of GC cells declined after interference in linc01555 expression. It was found in colony formation assay that the proliferation ability of GC cells declined after interference in linc01555 expression, and it was observed in wound healing assay that the cell migration ability in the experimental group was weakened compared with that in the control group. According to the results of transwell assay, both migration and invasion ability of GC cells declined after interference in linc01555 expression. Finally, the western blotting showed that there were changes in the expressions of molecular markers in the Notch signaling pathway after interference in linc01555 expression. Conclusions The expression of linc01555 is upregulated in GC tissues and cells, and the highly-expressed linc01555 promotes the proliferation, invasion and metastasis of GC cells through the Notch signaling pathway.Purpose Gastric cancer causes significant human mortality and is the fourth prevalent type of cancer across the globe. The gastric cancer treatment is hurdled by late diagnosis due to unavailability of biomarkers, lack of potent therapeutic targets and adverse effects of chemotherapy. Recent reports have indicated that miR-24 acts a tumor suppressor in different cancers. This study explored the role and therapeutic implications of miR-24 in gastric cancer. Methods Expression analysis was carried out in gastric cancer tissues and cell lines by qRT-PCR. Proliferation rate was monitored by WST-1 assay. Transwell assay was used to determine cell invasion and wound healing assay was used for cell migration. Protein expression analysis was carried out by western blot analysis. Results The results showed that miR-24 was significantly suppressed in gastric cancer tissues and cell lines. Overexpression of miR-24 in SNU-1 gastric cancer cells resulted in decline of proliferation rate in a time-dependent manner. In silico analysis together with the dual luciferase assay revealed RNA binding protein DND1 to be the target of miR-24.