Meanwhile, the mRNA and protein expression of JUNB and VEGF was determined by PCR, ELISA and western blot analyses. Of note, miR‑3133 overexpression downregulated, while miR‑3133 knockdown elevated the expression of JUNB and VEGF significantly. Furthermore, it was demonstrated that JUNB upregulated the expression and secretion of VEGF to promote HUVEC proliferation and angiogenesis. miR‑3133 was able to inhibit the effect of JUNB overexpression to promote cell proliferation, angiogenesis and the expression of VEGF. In conclusion, the present study demonstrated that miR‑3133 regulated endothelial cell proliferation and angiogenesis through the JUNB/VEGF pathway, which may provide an approach for inhibiting diaphragm formation of the inferior vena cava in MOVC.Lung carcinoma is a prominent cause of mortality among patients with cancer. Previous studies have reported the vital role of long non‑coding RNAs (lncRNAs) in the malignant progression of lung cancer. lncRNA RP11‑284F21.9 was originally identified to be expressed in lung carcinoma, but its specific function remains unknown. Therefore, the present study aimed to elucidate the role of lncRNA RP11‑284F21.9 in lung carcinoma progression. The expression of RP11‑284F21.9 in lung cell lines and tissues was measured using reverse transcription‑quantitative PCR. The endogenous expression of RP11‑284F21.9 was silenced using RNA interference, and cell viabilities were measured with a Cell Counting Kit‑8 assay. The invasion and apoptosis of cells were determined via Transwell assays and flow cytometry, respectively. The protein expression levels were measured by western blotting. An increased expression of RP11‑284F21.9 was identified in both lung carcinoma tissues and cells. Knockdown of RP11‑284F21.9 in lung carcinoma cells inhibited cell proliferation and invasion, but promoted cell apoptosis. The present study identified the existence of a direct interaction between RP11‑284F21.9 and microRNA (miRNA/miR)‑627‑3p. Mechanistically, it was demonstrated that RP11‑284F21.9 promoted the proliferation and invasiveness of lung carcinoma cells, in part, via the regulation of miR‑627‑3p. Furthermore, cell division cycle and apoptosis regulator 1 (CCAR1) was identified as a target gene of miR‑627‑3p. The in vivo tumor growth assay also demonstrated that the knockdown of RP11‑284F21.9 suppressed tumor growth, upregulated miR‑627‑3p and downregulated CCAR1 in the xenograft model of nude mice. Thus, the present findings indicated the tumor promoting functions of RP11‑284F21.9 in the progression of lung carcinoma, and provided a novel lncRNA/miRNA axis as a target for the management of lung cancer.Propofol is frequently used for anesthesia in cancer surgery. It has been suggested that treatment with propofol serves a tumor‑suppressing role in human gastric cancer (GC). Therefore, the present study aimed to explore the potential mechanism of propofol in GC. In the present study, GC cell lines (HGC‑27 and AGS) were treated with various concentrations of propofol, and an MTT assay was performed to detect the cell viability. In addition, flow cytometry and Transwell assays were used to evaluate the apoptosis and invasive ability of GC cells, respectively. Western blotting was performed to detect the protein levels of cyclin‑dependent kinase inhibitor P21 (P21), B‑cell lymphoma‑2 (Bcl‑2), matrix metalloproteinase 9 (MMP9) and E26 oncogene homolog 1 (ETS1). Furthermore, reverse transcription‑quantitative PCR was used to examine the expression levels of circular RNA‑PVT1 (circ‑PVT1), micoRNA‑195‑5p (miR‑195‑5p) and ETS1 in GC tissues and cells. The target interaction between miR‑195‑5p and circ‑PVT1 or ETS1 wi‑circ‑PVT1‑induced low expression of ETS1. Downregulation of ETS1 induced by propofol in HGC‑27 and AGS cells could be restored by circ‑PVT1 upregulation or miR‑195‑5p silencing. Circ‑PVT1 silencing facilitated the propofol‑induced anti‑GC effect in vivo. In conclusion, the present study indicated that propofol inhibited the proliferation and invasion, but enhanced the apoptosis of GC cells by regulating the circ‑PVT1/miR‑195‑5p/ETS1 axis.Extranodal natural killer (NK)/T cell lymphoma, nasal type (ENKL) is a rare type of non‑Hodgkin's lymphoma that is associated with limited effective treatment options and unfavorable survival rate, which is partly the result of multidrug resistance (MDR). The presence of side population (SP) cells‑SNK‑6/ADM‑SP (SSP) cells has been previously used to explore mechanisms of drug resistance. ATP‑binding cassette subfamily G member 2 (ABCG2) is a gene involved in MDR and is closely associated with SPs. However, the function of ABCG2 in SSP cells is unclear. The present study verified the high expression of ABCG2 in SSP cells. The IC50 values of doxorubicin, cytarabine, cisplatin, gemcitabine and l‑asparaginase were tested to evaluate drug sensitivity in SSP cells with different levels of ABCG2 expression. ABCG2 was identified as a gene promoting in MDR. ABCG2 upregulated cell proliferation, increased clonogenicity, increased invasive ability and decreased apoptosis, in vivo and in vitro, when cells were treated with gemcitabine. To conclude, ABCG2 enhanced MDR and increased the typical biological characteristics associated with cancer cells in SP cells.  https://www.selleckchem.com/products/tenapanor.html  With further investigation of the ABCG2 gene could have the potential to reverse MDR in ENKL.In recent years, an increasing number of long non‑coding RNAs (lncRNAs) have been discovered using microarrays and nucleic acid sequencing technology. LncRNAs exert crucial biological functions by regulating signaling pathways. In particular, the lncRNA growth arrest‑specific transcript 5 (GAS5) has been documented to serve a crucial role in numerous signaling pathways. This article discusses the latest developments in the association between GAS5 and microRNA (miRNA), p53, mTOR, glucocorticoid response element (GRE) and AKT in order to investigate the roles served by GAS5. miRNAs can activate related signaling pathways and GAS5 can combine with miRNA to regulate related signaling pathways. GAS5 may regulate p53 expression via derivation of snoRNA, but the underlying mechanism requires further investigation. GAS5 overxpresion reduces the expression level of mTOR, which is induced by inhibiting miR‑106a‑5p expression. GAS5 is a sponge of GR, and serves a role in controlling and maintaining glucocorticoid sensitivity and drug resistance via competitive combination with GR.