B-Myb is an important transcription factor that plays a critical role in gene expression regulation and tumorigenesis. However, its functional implication in colorectal cancer remains elusive. In this study, we found that B-Myb was significantly upregulated at both mRNA and protein levels in colorectal cancer samples compared to non-tumor counterparts. B-Myb overexpression accelerated cell proliferation, cell cycle progression and cell motility in colorectal cancer cells, and promoted tumor growth in orthotopic nude mouse models in vivo. In contrast, B-Myb depletion inhibited these malignant phenotypes. Mechanistic investigations revealed that E2F2 was a novel transcriptional target of B-Myb and is essential to B-Myb-induced malignant phenotypes. Notably, B-Myb and E2F2 exhibited positive expression correlation, and interacted with each other in colorectal cancer cells. In addition to their autoregulatory mechanisms, B-Myb and E2F2 can also directly transactivate each other, thus constituting consolidated reciprocal feed-forward transactivation loops. Moreover, both B-Myb and E2F2 are required for the activation of ERK and AKT signaling pathways in colorectal cancer cells. Taken together, our data clarified a critical role for B-Myb in colorectal cancer and unraveled an exquisite mutual collaboration and reciprocal cross regulation between B-Myb and E2F2 that contribute to the malignant progression of human colorectal cancer.

ACER2 is a critical sphingolipid metabolizing enzyme, and has been shown to be remarkably up-regulated following various stimuli such as DNA damage. However, the transcriptional regulatory mechanism of ACER2 gene and its potential role in the regulation of autophagy remain unknown. In this study, we have for the first time identified the human ACER2 gene promoter, and found that human ACER2 transcription is directly regulated by p53 and ACER2 is implicated in the induction of autophagy as well as apoptosis. A series of luciferase reporter assay demonstrated that ACER2 major promoter is located within its first intron where the consensus p53-binding sites exist. Consistently, forced expression of p53 significantly stimulated ACER2 transcription. Notably, p53-mediated autophagy and apoptosis were markedly enhanced by ACER2. Depletion of the essential autophagy gene ATG5 revealed that ACER2-induced autophagy facilitates its effect on apoptosis. Further studies clearly showed that ACER2-mediated autophagy and apoptosis are accompanied by ROS generation. In summary, our present study strongly suggests that ACER2 plays a pivotal role in p53-induced autophagy and apoptosis, and thus might serve as a novel and attractive molecular target for cancer treatment.

Background Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. Methods Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively. Results Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death. Conclusions Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition.

Elastase is a type of protease that specifically degrades elastin. It has broad application prospects in medicine, food industry, and daily-use chemical industry. In this study, we isolated a bacterial strain WZE87 with high elastin-hydrolysis activity, which was identified as Chryseobacterium indologenes based on morphology, physiological and biochemical characteristics, and 16S rDNA sequence analysis. The elastase produced by this strain was purified by three steps: ammonium sulfate precipitation, Q-Sepharose fast-flow anion-exchange chromatography, and Sephadex G-75 gel-filtration chromatography. The purified elastase was 2376.5 U/mg in activity (a 8.3-fold increase in specific activity), and the recovery was 5.8%. Its molecular mass was estimated to be 26 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. This enzyme was stable in the pH range of 5.0-10.5 at 37°C. The optimal temperature and pH were 37°C and 7.5, respectively. The activity of this elastase was found to decrease when the temperature was higher than 50°C. The activity was also inhibited by Zn 2? , Fe 2? , Fe 3? , and Mn 2? ions. The specific hydrolytic ability of this enzyme was similar to that of papain on substrates like gelatin, casein, soybean-isolated protein and bovine hemoglobin. However, this elastase preferentially hydrolyzed elastin in a protein mixture because of its specific adsorption. Considering its promising properties, this protease may be considered a potential candidate for applications in related industries.

Plant‐specific NAC (NAM, ATAF1/2, and CUC2) transcription factors (TFs) play important roles in various stress responses. However, the characteristics and functions of NAC TFs in Tartary buckwheat [Fagopyrum tataricum (L.) Gaertn.], an important pseudocereal crop that is strongly adapted to growth in adverse environments, have not been investigated. Here, eight NAC‐like genes, termed FtNAC2 through FtNAC9, were isolated and characterized from Tartary buckwheat. Amino acid sequence alignment analysis demonstrated that all the FtNAC proteins contain typical NAM domain of the NAC TFs family in the N terminus. Phylogenetic analysis showed that the eight FtNAC TFs were assigned to three abiotic stress‐related functional subgroups. To investigate their roles in response to stresses, the relative expression levels of FtNAC genes were analyzed under abiotic stresses (salt, drought, cold, and ultraviolet B) and exogenous phytohormones (abscisic acid, methyl jasmonate, and salicylic acid) treatments. All the FtNAC genes responded to one or more treatments, among which FtNAC4 and FtNAC7 showed >20‐fold upregulation of messenger RNA levels in response to salt, drought, abscisic acid, and salicylic acid treatments. The expression analysis of the NAC gene family in Tartary buckwheat under abiotic stress open the way to further investigate the molecular mechanism of NAC‐dependent transcriptional control of stress response.