Hein Marcussen (enemyparty44)

For OS, TSP-manual HR=1.512 (95% CI 1.045-2.187); TSP-cad HR=1.443 (95% CI 0.993-2.097) and TSP-cad(median) HR=1.632 (95% CI 1.105-2.410). Fortunately, TSP-manual and TSP-cad were also found independent prognostic factor in all the cohorts. It was found that TSP-cad had slightly higher HR and wider CI than TSP-manual. Conclusions Our research showed that TSP was an independent prognostic factor in CRC. Moreover, threshold algorithm for the quantitation of TSP could be established. In conclusion, with this Rapid multi-dynamic threshold Algorithm for Gray Image counting of TSP, which showed a higher accuracy than manual evaluation by pathologists and could be a practical method for CRC to guide clinical decision making.Mounting evidence indicates that long non-coding RNAs influence the progression of cervical cancer, but the precise function of LINC01503 in the pathogenesis of the disease remains unknown. Here, we found higher levels of LINC01503 in cervical cancer tissues. High LINC01503 expression was associated with enhanced progression of cervical cancer as indicated by advanced FIGO stage, increased metastasis of tumor cells to lymph nodes, and invasion into deeper cervical tissues. LINC01503 inhibition markedly suppressed the invasion and proliferative ability of tumor cells. Mechanistically, LINC01503 was demonstrated to negatively modulate the expression of miR-615-3p in cervical cancer. CCND1 was found to be a target of miR-615-3p. Rescue experiments indicated that LINC01503 inhibition suppressed the invasion and proliferative ability of the tumor cells, a phenomenon that was reversed following miR-615-3p inhibition or CCND1 overexpression. Collectively, these data indicate that LINC01503 enhances the progression of cervical cancer cells via interaction with miR-615-3p/CCND1 axis.Tumor distant metastasis is the primary cause of death in colorectal cancer (CRC) patients. GL-V9 is a newly synthesized flavonoid derivative with several beneficial biological functions including anti-tumor and anti-inflammation. However, the anti-metastatic effect of GL-V9 and related mechanisms in CRC remains unknown. In this study, the anti-invasive and anti-migratory activities of GL-V9 were investigated in CRC cells. Using MTT assay, cell wound healing assay, and transwell migration assay, we showed that GL-V9 suppressed CRC cell viability, migration, and invasion in a concentration-dependent manner. In addition, the protein expression levels as well as activities of matrix metalloproteinase-2 (MMP-2) and matrix metalloproteinase-9 (MMP-9) were significantly reduced after GL-V9 treatment. Further analysis of the underlying mechanism revealed that GL-V9 inhibited PI3K/Akt signaling pathway upstream of MMP-2 and MMP-9. In conclusion, our study demonstrated that GL-V9 could suppress CRC cell invasion and migration through PI3K/Ak and MMP-2/9 axis. Therefore, GL-V9 might be a potential novel therapeutic agent against CRC metastasis.Purpose Several studies have indicated that SLC39A7 plays an important role in tumor progression; however, little is known about the function and mechanism of SLC39A7 in glioma. In this study, we aimed to explore the role of SLC39A7 in glioma development. Patients and methods Bioinformatic analysis was used to predict the role of SLC39A7 in glioma. Cell viability and Edu assays were used to detect the proliferation of glioma cells. A transwell assay was used to measure the invasion and migration of glioma cells. Western blotting, qPCR and ELISA were used to detect the expression of all molecules. Results SLC39A7 was found to be highly expressed in high-grade glioma patients with a poor prognosis. Our results indicated that SLC39A7 significantly promoted the proliferation, invasion and migration of glioma cells. Furthermore, SLC39A7 promoted tumorigenesis in orthotopic models. We determined that SLC39A7 promotes the malignant behaviors of glioma by activating the TNF-α-mediated NF-κB signaling pathway. Conclusion