Background/aimsThe dysregulation of circABCB10 may play an critical role in tumor progression. However, its function in liver cancer (HCC) is still unclear. Therefore, this experimental design is based on circABCB10 to explore the pathogenesis of HCC.MethodsThe expression of circABCB10 and miR-670-3p in HCC tissues was detected by RT-qPCR. CCK-8, Brdu incorporation, colony formation and transwell assays were used to determine the effect of circABCB10 on HCC cell proliferation and migration. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes of circABCB10 and miR-670-3p. HMG20A expression was detected by RT-qPCR and Western blotting. The tumor changes in mice were detected by in nude mice.ResultsCircABCB10 was significantly increased in HCC tissues and cell lines, and high CircABCB10 expression was directly associated with low survival in HCC patients. Silencing of circABCB10 inhibited proliferation and invasion of hepatocellular carcinoma. In addition, circABCB10 acted as a sponge of miR-670-3p to upregulate HMG20A expression. In addition, overexpression of miR-670-3p or knockdown of HMG20A reversed the carcinogenic effects of circABCB10 in HCC. There was a negative correlation between the expression of circABCB10 and miR-670-3p, and a positive correlation between the expression of circABCB10 and HMG20A in HCC tissues.ConclusioncircABCB10 promoted HCC progression by modulating the miR-670-3p/HMG20A axis, and circABCB10 may be a potential therapeutic target for HCC.Trail registration JL1H384739, registered at Sep 09, 2014.

To establish a simple and safe method for the preparation of paclitaxel PEG-PLGA nanoparticles emulsified in tpgs (PTX-pegpllga-np), for high drug loading; and to study its effect on proliferation and apoptosis of human pancreatic cancer cell line MIAPACA-2. PTX-PEG-PLGA-NP was prepared by one-step precipitation, using tpgs as emulsifier. The drug loading and particle size were used as an index to optimize the formulation, and the physical and chemical properties such as in vitro release and stability were characterized. The uptake of fluorescein coumarin 6 (C6) loaded PEG-PLGA-NP by MIAPACA-2 cells was observed by fluorescence microscope, and the growth and apoptosis of MIAPACA-2 cells after PTX-PEG-PLGA-NP were detected by MTT and flow cytometry respectively. The entrapment efficiency of the nanoparticles was 90.26%, the drug loading was 10.13%, the average particle size was 92.3±3.1 nm, and the zeta potential was 10.48±1.54 mV. The cumulative releases of nano preparation and general preparation (Taxol injection) in four hours were 25.9% and 98.5%, respectively; and the former had a strong sustained-release effect. The results of cell uptake experiments showed that the uptake of c6-PEG-PLGA-NP by MIAPACA-2 cells increased gradually with time. MTT results showed that PTX-PEG-PLGA-NP had no significant difference in the inhibition rate of MIAPACA-2 cells compared with PTX group. Flow cytometry showed that PTX-PEG-PLGAnp was superior better than PTX in inducing apoptosis in MIAPACA-2 cells. The tpgs emulsification method is simple and environment-friendly. The paclitaxel loaded nanoparticles prepared through the optimization of the formulation have large drug loading capacity and uniform particle size, which can target the pancreatic cancer MIAPACA-2 cells, and do not weaken its ability to inhibit the growth of MIAPACA-2 cells. The nanoparticles also induce apoptosis in cancer MIAPACA-2 cells, and could be used for further clinical treatment of pancreatic cancer.

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12935-020-01586-0.

Hepatocellular carcinoma (HCC) consist in a proinflammatory tumor environment that is characterized by the presence of many chemokines and cytokines. Expression of CCL17 associated with diagnoses and poor prognosis in different cancers. There are few investigations indicated the relationship between CCL17 and HCC. Thus, this study aims to investigate the role of CCL17 in HCC progression. qRT-PCR and Western Blot were performed to detect expression of CCL17 in HCC cell lines and normal hepatocyte. Elisa was used to determine TNFα, IL-6 and IL-1β. Wound-healing assay and Transwell assay were performed to assed cell metastasis. CCL17 signaling was examined utilizing Western Blot. Here, we showed that CCL17 levels markedly increased in HCC cell lines. At the same time, TNFα, IL-6 and IL-1 β were increased time-dependent after treating human recombinant CCL17 protein. Cell metastasis was significantly promoted by CCL17 while TNFa inhibitor (Lenalidomide) reversed the effects of CCL17. NF-κB signaling pathway was activated by CCL17 and TNFα inhibitor suppressed the effects of CCL17. In conclusion, CCL17 promoted cell metastasis via TNFα/NF-κB signaling pathway. CCL17 may be a potential biomarker for HCC progression.