The S100 protein family member S100A4 regulates various cellular functions. Previous studies have shown that elevated expression of S100A4 is associated with progression and metastasis of colorectal cancer (CRC). However, little is known about whether and how S100A4 contributes to CRC development. In our present study, the elevated expression of S100A4 in CRC tissues compared to matched adjacent normal tissues was confirmed by immunohistochemistry, semi-quantitative RT-PCR and Western blot. Adenovirus-mediated S100A4 overexpression obviously enhanced viability and migration of CRC cells, which was detected by MTT assay and transwell assay, respectively. Additionally, S100A4 overexpression increased the phosphorylation levels of Akt, mTOR and p70S6K. These effects of S100A4 were abolished by treatment with either the specific PI3K/Akt inhibitor LY294002, or the specific mTOR/p70S6K inhibitor rapamycin. Furthermore, overexpression of S100A4 resulted in upregulation of VEGF and downregulation of E-cadherin, which were strongly reversed by either LY294002 or rapamycin. Altogether, our results demonstrate that activation of the PI3K/Akt/mTOR/p70S6K signaling pathway is involved in S100A4-induced viability, migration, upregulation of VEGF and downregulation of E-cadherin in CRC cells.

The S100A6 protein, a member of the S100 protein family, is overexpressed in many tumors including colorectal carcinoma (CRC). Although recent studies showed that the elevated expression of S100A6 was associated with the stage and lymphatic permeation of CRC, little is known about whether and how S100A6 contributes to CRC development. Here we investigated the S100A6 expression in CRC tissues and cell lines, and explored the molecular mechanisms underlying the role of S100A6 in CRC development by examining cell proliferation and migration in vitro, and tumorigenicity in nude mice. The results show that S100A6 expression was markedly increased in CRC tissues and cell lines compared to normal colon tissues and a normal colon mucosal epithelial cell line, respectively. Recombinant adenovirus-mediated overexpression of S100A6 or treatment with recombinant S100A6 protein in HCT116, a CRC cell line with relative low S100A6 expression, resulted in enhanced cell proliferation and migration, and the mitogen-activated protein kinase (MAPK) activation in vitro, and tumor growth in vivo. Conversely, RNAi-mediated knockdown of S100A6 in LoVo, a CRC cell line with relative high S100A6 expression, resulted in reduced cell proliferation, migration and MAPK activity. S100A6-induced proliferation was partially attenuated by an ERK inhibitor while migration was suppressed by a p38 inhibitor. Taken together, our results suggest that the cellular effects of S100A6 are mediated by the ERK and p38 MAPK pathways, and modulation of these pathways may be employed for CRC prevention and therapy.

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The ion valence state, phase composition, microstructure, and microwave dielectric properties of Sr(1−1.5x)CexTiO3 (x = 0.1–0.67, SCT) ceramics were systematically investigated. Sr(1−1.5x)CexTiO3 ceramics were produced with gradual structural evolution from a cubic to a tetragonal and turned to an orthorhombic structure in the range of 0.1 ≤ x ≤ 0.67. Above a critical Ce proportion (x = 0.4), microstructural changes and normal grain growth initially occurred. On the basis of chemical analysis results, the reduction of Ti4+ ions was hastened by tetravalent ions (Ce4+). By contrast, this reduction was inhibited by trivalent ions (Ce3+). The observed dielectric behavior was strongly influenced by phase composition, oxygen vacancies (VnormalO∙∙), and defect dipoles, namely, (Ti′−VO∙∙) and (VSr″−VO∙∙). Temperature stable ceramics sintered at 1350°C for 3 h in air yielded an intermediate value of dielectric constant (εr = 40), with the smallest reported value of temperature coefficient of resonant frequency (τf = +0.9 ppm/°C), and quality factor (Q × f = 5699 GHz) at x = 0.6.

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