The biochemical characteristics of <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350.

<p>The biochemical characteristics of <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350.</p

Microbial strains used in this study.

<p>Microbial strains used in this study.</p

Results of enterotoxin detection.

<p>Results of enterotoxin detection.</p

Growth curves and ZEN degradation kinetics of <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 in corn meal medium containing 1.56 ppm ZEN.

<p>The bars represent standard errors of the means.</p

Primers used for PCR in this study.

<p>Primers used for PCR in this study.</p

Growth curves <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 cultured in LB broth with or without ZEN (3.5 ppm), and ZEN degradation kinetics of <i>B</i>. <i>amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 in LB broth with ZEN (3.5 ppm).

<p>The bars represent standard errors of the means.</p

ZEN degradation kinetics of <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 in phosphate-buffered saline (PBS; 0.1 M, pH 7.0) containing 5 ppm of ZEN.

<p>ZEN degradation kinetics of <i>Bacillus amyloliquefaciens</i> LN and <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 in phosphate-buffered saline (PBS; 0.1 M, pH 7.0) containing 5 ppm of ZEN.</p

Neighbor-joining phylogenetic tree-based study of the V1-V3 region of the 16S rRNA gene of <i>Bacillus</i> species.

<p>At major nodes, bootstrap percentages for 1,000 re-samplings are shown. The scale bar represents 0.1 nucleotide substitution per nucleotide position. <i>Bacillus</i> species include <i>Bacillus aerophilus</i> 28K (GenBank accession no. AJ831844), <i>B</i>. <i>altitudinis</i> 41KF2b (AJ831842), <i>B</i>. <i>amyloliquefaciens</i> BCRC 11601 (NR_116022), <i>B</i>. <i>amyloliquefaciens</i> ATCC 23350 (X60605), <i>B</i>. <i>amyloliquefaciens</i> LN (KP261025), <i>B</i>. <i>anthracis</i> ATCC 14578 (KC119183), <i>B</i>. <i>licheniformis</i> DSM 13 (X68416), <i>B</i>. <i>mojavensis</i> CR-95 (AY603656), <i>B</i>. <i>mycoides</i> ATCC 6462 (NR_115993), <i>B</i>. <i>pseudomycoides</i> JCM 12231 (LC107614), <i>B</i>. <i>pumilus</i> ATCC 7061 (AY876289), <i>B</i>. <i>safensis</i> FO-036b (AF234854), <i>B</i>. <i>sonorensis</i> NRRL B-23154 (NR_025130), <i>B</i>. <i>subtilis</i> subsp. <i>subtilis</i> DSM 10 (AJ276351), and <i>Bacillus thuringiensis</i> ATCC 10792 (NR_114581). <i>Pseudomonas aeruginosa</i> ATCC 10145 (NR_114471) was used as an outgroup to root the tree.</p

Estrogen Enhances the Cell Viability and Motility of Breast Cancer Cells through the ERα-ΔNp63-Integrin β4 Signaling Pathway

<div><p>Estrogen induces ERα-positive breast cancer aggressiveness via the promotion of cell proliferation and survival, the epithelial-mesenchymal transition, and stem-like properties. Integrin β4 signaling has been implicated in estrogen/ERα-induced tumorigenicity and anti-apoptosis; however, this signaling cascade poorly understood. ΔNp63, an N-terminally truncated isoform of the p63 transcription factor, functions as a transcription factor of integrinβ4 and therefore regulates cellular adhesion and survival. Therefore, the aim of the present study was to investigate the estrogen-induced interaction between ERα, ΔNp63 and integrin β4 in breast cancer cells. In ERα-positive MCF-7 cells, estrogen activated ERα transcription, which induced ΔNp63 expression. And ΔNp63 subsequently induced integrin β4 expression, which resulted in AKT phosphorylation and enhanced cell viability and motility. Conversely, there was no inductive effect of estrogen on ΔNp63-integrinβ4-AKT signaling or on cell viability and motility in ERα-negative MDA-MB-231 cells. ΔNp63 knockdown abolishes these estrogen-induced effects and reduces cell viability and motility in MCF-7 cells. Nevertheless, ΔNp63 knockdown also inhibited cell migration in MDA-MB-231 cells through reducing integrin β4 expression and AKT phosphorylation. In conclusion, estrogen enhances ERα-positive breast cancer cell viability and motility through activating the ERα-ΔNp63-integrin β4 signaling pathway to induce AKT phosphorylated activation. Those findings should be useful to elucidate the crosstalk between estrogen/ER signaling and ΔNp63 signaling and provide novel insights into the effects of estrogen on breast cancer progression.</p></div

Pseudopodium patterns of co-treatment of estrogen and ΔNp63 knockdown.

<p>After siΔNp63 or scrambled siRNA was transfected into MCF-7 cells for 48 h, the cells were co-treated with 10nM estrogen or 0.1% ethanol. A wound-healing assay was conducted to compare the pseudopodium patterns at 24 h. Only the cells treated with 10nM estrogen showed protruding pseudopodia, and siΔNp63 reduced the pseudopodium patterns, regardless of the presence or absence of estrogen.</p