Accumulating studies indicates that circular RNAs (circRNAs) play an imperative role in modulating cancer progression and metastasis. In the previous study,
In this work, we reported a facile wet chemical method for depositing Pt nanoparticles on the surface of boron nitride nanosheets (BNNS-Pt NPs). The deposited nanocomposite was applied for glassy carbon electrode surface modification. The modified electrode was then used for detecting ursolic acid (UA). The results indicate that the BNNS-Pt NPs exhibited excellent electrocatalytic activity toward UA oxidation compared with that of the bare glassy carbon electrode (GCE) and Pt NPs/GCE. The UA oxidation currents is linearly related its concentration from 1 to 1,200 pM. The limit of detection can be calculated to be 0.5 pM. In addition, the UA sensor was also successfully used for the determination of UA in Ligustri lucidum fruit samples.
Objective To investigate the function and the mechanism of miR-125b in the invasion and metastasis of gastric cancer and provide experimental basis for finding and developing new therapeutic strategies for gastric cancer. Methods The difference of miR-125b expression in gastric cancer tissues and adjacent tissues was detected by qRT-PCR. The same test was performed in different gastric cancer cell lines. The effect of miR-125b on SGC-7901 and BGC-823 gastric cancer cell viability was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Transwell assay was used to detect the effect of miR-125b on invasion and metastasis of gastric cancer cells. The target gene STAT3 of miR-125b was identified and validated by dual luciferase reporter assay. Western blot assay and immunofluorescence staining were used to detect the effect of miR-125b on the expression and distribution of STAT3 protein. The inhibitor and activator of STAT3 were used to confirm the effect of STAT3 on invasion and metastasis of gastric cancer cells. Peritoneal metastasis experiment and IHC were used to study the inhibitory effect of miR-125b on the metastasis of gastric cancer in vivo. Results The results of qRT-PCR showed that 125b expression was significantly lower in gastric cancer than in adjacent tissues, which indicated poor prognosis for gastric-cancer patients. Furthermore, two gastric-cancer cell lines, SGC-7901 and BGC-823, exhibited lower miR-125b levels than the normal cell line HEK293. After treatment with miR-125b mimics, cell proliferation was markedly inhibited. Meanwhile, the invasion and metastasis of gastric cancer cells were also inhibited after treated with miR-125b mimics. We also identified the signal transducer and activator of transcription 3 (STAT3) as a potential target of miR-125b based on patient data from The Cancer Genome Atlas (TCGA). Dual luciferase assays revealed that miR-125b directly inhibited STAT3 by binding to its 3′-untranslated region (UTR). Immunofluorescence assay showed that miR-125b could affect the subcellular distribution of STAT3. Moreover, treatment with miR-125b mimics or stattic inhibited invasion and migration in the gastric cancer cell lines, and IL-6 could reverse the inhibitory effect. Finally, nude mice xenografted with gastric-cancer cells expressing miR-125b mimics exhibited smaller tumors and lower transfer rates than mice engrafted with control group cells. Conclusion These data suggested that miR-125b inhibited invasion and metastasis in gastric cancer by inhibiting STAT3; therefore, miR-125b and STAT3 could be potential therapeutic targets in the treatment of gastric cancer.
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