Anti-CDK4 (full length) polyclonal antibody

To preserve bioactivity and achieve colon targeted release of phycocyanin (PC), the polysaccharides-based electrospun fiber mat (EFM) containing PC and prebiotics was prepared and characterized. In vitro release tests confirmed the colon targeting behavior of PC, in particular, faster release of PC was achieved due to the addition of prebiotics. Ritger-Peppas model confirmed that the release of PC in simulated colon fluids follows a mechanism of anomalous transport (non-Fickian). CCK-8 results showed that the combination of PC and prebiotics exerted a significant anti proliferative effect on HCT116 cells with an 1050 values of 22.31, 17.12 and 11.63 mg/mL after 24, 48, and 72 h, respectively. Furthermore, the cell cycle and apoptosis analysis revealed that the inhibition activity on Hal16 cells was caused by arresting cell cycle at G0/G1 phase that is relevant to the inhibition of cyclin D1 and CDK4 and the up-regulation of p21 expression, and inducing cell apoptosis by mediating the mitochondrial pathway as well, in which the decrease of Bcl-2/Bax, activation of caspase 3 and release of cytochrome c were included. This study suggests that the PC-loaded EFM with GOS holds a great potential as an effective formulation for colon cancer prevention. (C) 2020 Elsevier B.V. All rights reserved.

Aberrant expression of miR-1256 has been reported to be closely associated with the development and progression of tumors, including colon cancer and lung cancer. However, study of its expression pattern and functional role in papillary thyroid cancer (PTC) is rare. Using quantitative real time PCR analysis, we found miR-1256 was significantly down-regulated in PTC tissues and cell lines. The correlation of miR-1256 expression with clinicopathological features was statistically analyzed. The results showed miR-1256 expression was significantly correlated with tumor size (p = 0.0124) and TNM stage (p = 0.0032). Restoring miR-1256 expression significantly inhibited proliferation and cell cycle progression of PTC cells demonstrated by CCK-8 and flow cytometry assays. Luciferase reporter assay and biotin-avidin pull-down assay showed miR-1256 can directly target 5-hydroxytryptamine receptor 3A (HTR3A) in PTC cells. The expression of miR-1256 was inversely correlated with HTR3A expression in PTC tissues. Knockdown of HTR3A imitated the suppressive effects of miR-1256 in PTC cells. Ectopic expression of HTR3A can antagonize the effects of miR-1256 on PTC cells. Furthermore, the suppressive effects of miR-1256 on the expression of PCNA, CDK4, Cyclin D1, and p21 were partially reversed by HTR3A overexpression in PTC cells. In summary, our data suggested that miR-1256 could suppress PTC cellular function by targeting HTR3A, which might be a potential therapeutic target for patients with PTC.