14-3-3epsilon contributes to tumour suppression in laryngeal carcinoma by affecting apoptosis and invasion

<p>Abstract</p> <p>Background</p> <p>14-3-3epsilon regulates a wide range of biological processes, including cell cycle control, proliferation, and apoptosis, and plays a significant role in neurogenesis and the formation of malignant tumours. However, the exact function and regulatory mechanism of 14-3-3epsilon in carcinogenesis have not been elucidated.</p> <p>Methods</p> <p>The expression of <it>14-3-3epsilon </it>was assessed by RT-PCR and western blotting. The invasiveness and viability of Hep-2 cells were determined by the transwell migration assay and MTT assay, respectively. Cell cycle and apoptosis of Hep-2 cells were detected by flow cytometry.</p> <p>Results</p> <p>The mRNA and protein expression of <it>14-3-3epsilon </it>in larynx squamous cell carcinoma (LSCC) tissues were significantly lower than those in clear surgical margin tissues. Statistical analysis showed that the 14-3-3epsilon protein level in metastatic lymph nodes was lower than that in paired tumour tissues. In addition, the protein level of 14-3-3epsilon in stage III or IV tumours was significantly lower than that in stage I or II tumours. Compared with control Hep-2 cells, the percentages of viable cells in the 14-3-3epsilon-GFP and negative control GFP groups were 36.68 ± 14.09% and 71.68 ± 12.10%, respectively. The proportions of S phase were 22.47 ± 3.36%, 28.17 ± 3.97% and 46.15 ± 6.82%, and the apoptotic sub-G1 populations were 1.23 ± 1.02%, 2.92 ± 1.59% and 13.72 ± 3.89% in the control, negative control GFP and 14-3-3epsilon-GFP groups, respectively. The percentages of the apoptotic cells were 0.84 ± 0.25%, 1.08 ± 0.24% and 2.93 ± 0.13% in the control, negative control GFP and 14-3-3epsilon-GFP groups, respectively. The numbers of cells that penetrated the filter membrane in the control, negative control GFP and 14-3-3epsilon-GFP groups were 20.65 ± 1.94, 17.63 ± 1.04 and 9.1 ± 0.24, respectively, indicating significant differences among the different groups.</p> <p>Conclusions</p> <p>Decreased expression of <it>14-3-3epsilon </it>in LSCC tissues contributes to the initiation and progression of LSCC. <it>14-3-3epsilon </it>can promote apoptosis and inhibit the invasiveness of LSCC.</p

Pre-clinical Models of Pancreatic Ductal Adenocarcinoma

Pancreatic ductal adenocarcinoma (PDA) is one of the most difficult human malignancies to treat. Five-year survival rate of PDA patients is 7%, and PDA is predicted to become the second leading cancer-related cause of death in the United States of America. Despite intensive efforts, the translation of findings in preclinical studies has been ineffective, due partially to the lack of preclinical models that faithfully recapitulate features of human PDA. Here we review current preclinical models for human PDA (e.g. human PDA cell lines, cell line-based xenografts and patient-derived tumor xenografts). In addition, we discuss potential applications of the recently developed pancreatic ductal organoids, three-dimensional culture systems and organoid-based xenografts as new preclinical models for PDA

Minute virus of mice inhibits cell transformation by simian virus 40.

Certain paroviruses have been reported to inhibit spontaneous or virus-induced tumorigenesis in rodents; the mechanisms of this antineoplastic activity is unknown. We have investigated the ability of the minute virus of mice (MVM), a non-defective paravirus, to interfere with the in vitro transformation of mouse cells by simian virus 40 (SV40). We used variants of BALB/c 3T3 cells, denoted PVR, selected for their resistance to the lytic effect of MVM. We report here that inoculation of SV40-infected PVR cells with MVM reduced dramatically the yield of transformed clones. Moreover, stable SV40 transformants of PVR cells lost up to 85% of their ability to grow in soft agar after MVM infection. Our results indicate that the antineoplastic effect of parvoviruses can be simulated in cell cultures and may involve a direct and selective toxic effect of these viruses on malignant cells or their precursors.SCOPUS: ar.jinfo:eu-repo/semantics/publishe