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Chronic low dose of tumor necrosis factor- α (TNF- α) stimulation promotes tumorigenesis by facilitating tumor proliferation and metastasis. The plasma levels of TNF- α are increased in patients with renal cell carcinoma (RCC). Furthermore, high-grade clear cell RCC cell lines secrete more TNF- α than low-grade ones, and allow low-grade cell lines' gain of invasive ability. However, the molecular mechanism of TNF- α in mediating progression of RCC cells remains unclear. In the present study, TNF- α induced epithelial–mesenchymal transition (EMT) of RCC cells by repressing E-cadherin, promoting invasiveness and activating matrix metalloproteinase (MMP) 9 activity. RCC cells underwent promoted growth in vivo following stimulation with TNF- α. In addition, TNF- α induced phosphorylation of extracellular signal-regulated kinase, nuclear factor kappa B (NF- κB) and Akt in a time-dependent manner, and increased nuclear translocation and promoter activity of NF- κB. To investigate the role of NF- κB activation in TNF- α-induced EMT of RCC, we employed chemical inhibitors (NF- κB activation inhibitor and Bay 11-7082) and transfected dominant-negative (pCMV-I κB αM) and overexpressive (pFLAG-p65) vectors of NF- κB. While overexpression of NF- κB p65 alone could induce E-cadherin loss in RCC, EMT phenotypes and MMP9 expressions induced by TNF- α were not reversed by the inhibitors of NF- κB activation. These results suggest that the TNF- α signaling pathway is involved in the tumorigenesis of RCC. However, NF- κB activation is not crucial for invasion and EMT enhanced by TNF- α in RCC cells.

Two new lactams, coixspirolactam D (1) and coixspirolactam E (2), and a new spiroenone, coixspiroenone (3), together with seven known compounds, coixspirolactam A (4), coixspirolactam B (5), coixspirolactam C (6), coixlactam (7), coixol (8), ethyl dioxindole-3-acetate (9), and isoindol-1-one (10), and two neolignans, zhepiresionol (11) and ficusal (12), were isolated from the bioactive subfraction of adlay bran ethanolic extract (ABE). Compounds 9 and 10 are the first isolates from natural resources. The structures of new compounds were identified by spectroscopic methods, including infrared (IR) spectrum, 1D and 2D nuclear magnetic resonance (NMR), and mass spectrum (MS). All of the isolated compounds were tested for antiproliferative effects on MCF-7, MDA-MB-231, and T-47D cells. Results showed that compounds 1, 3, 4, 6, and 7 at 50 μM significantly inhibited MCF-7 cell proliferation by 30.2, 19.2, 21.0, 13.5, and 32.4%, respectively; compounds 2, 4, and 7 significantly inhibited T-47D cells at 50 μM by 20.7, 24.8, and 28.9%; and compounds 1, 2, and 12 significantly inhibited MDA-MB-231 cells at 50 μM by 47.4, 25.3, and 69.3%, respectively. In conclusion, ABE has antiproliferative activities, and this effect is partially related to the presence of lactams and spiroenone.

A fast sensor was used as a vacuum gauge to measure the transit time of a gas pressure through an acoustic delay line (ADL). The results were compared with the predictions of two theoretical models. We found that in the rupture pressure range of 101 to 104 Pa, the predictions of Jean and Rauss’ model, based on the assumption that the flow of gas be a gas fluid, set lower boundaries for the observed transit times; while the predictions of our model, based on the molecular motion, set the upper ones.