The Arabidopsis UDP-glycosyltransferase75B1, conjugates abscisic acid and affects plant response to abiotic stresses

Plant Molecular Biology - This study revealed that the Arabidopsis UGT75B1 plays an important role in modulating ABA activity by glycosylation when confronting stress environments. The cellular ABA...     

Variation for Resistance to <i>Alternaria tenuissima</i> and Potential Structural Mechanism among Different Cultivars of <i>Chrysanthemum morifolium</i>

Black spot disease, caused by the necrotrophic fungus Alternaria tenuissima (Fr.) Wiltsh (A. tenuissima), is considered a highly destructive disease of Chrysanthemum (Chrysanthemum morifolium Ramat.). A set of 17 accessions of commercial chrysanthemum cultivars were evaluated for resistance to A. tenuissima by seedling artificial inoculation. It was found that the reaction of the accessions to artificial inoculation ranged from resistant to highly susceptible. Five varieties of chrysanthemum (‘Zhongshan Taogui’, ‘Jinba’, ‘Zhongshan Jinguan’, ‘Jinling Wanhuang’ and ‘Jinling Yangguang’) were resistant; two varieties of chrysanthemum (‘Zhongshan Xinggui’ and ‘Zhongshan Jinkui’) were moderately resistant; and others were susceptible to various degrees, four varieties of chrysanthemum (‘Zhongshan Zihe’, ‘Zhongshan Jiuhong’, ‘Zaoyihong’ and ‘Jinling Jiaohuang’) were highly susceptible, especially. Some leaf morphological features of two resistant and two highly susceptible cultivars were further researched. Trichome density, length, height, gland size and stomata density were found to be associated with plant passive resistance. Resistant varieties that were identified in present study will be promising germplasm for exploitation of breeding programmes aimed at developing A. tenuissima-resistant cultivars and increasing genetic diversity.     

What causes the differences in cavitation resistance of two shrubs? Wood anatomical explanations and reliability testing of vulnerability curves

Relationships between xylem anatomical traits and cavitation resistance have always been a major content of plant hydraulics. To know how plants cope with drought, it is extremely important to acquire detailed knowledge about xylem anatomical traits and assess the cavitation resistance accurately. This study aims to increase our knowledge in the methods determining cavitation resistance and xylem anatomical traits. We selected a semi-ring-porous species, Hippophae rhamnoides L., and a diffuse-porous species, Corylus heterophylla F., to clarify the reasons for the difference in cavitation resistance based on detailed xylem anatomical traits and reliable vulnerability curves (VCs). Both Cavitron and bench dehydration (BD) were used to construct VCs. Xylem anatomical traits, including pit membrane ultrastructure of these two species, were determined. The VCs obtained by the two different techniques were of different types for H. rhamnoides, its Cavitron VCs might be unreliable because of open-vessel artifacts. On the basis of BD VCs, H. rhamnoides showed higher cavitation resistance than C. heterophylla, and this is attributed to its low vessel connectivity as well as non-porous and thicker pit membranes.     

Extraction and Separation of Sinapine from Rapeseed Cake and the Mode of Action of Melanin Production Inhibition

Molecular Biology - Brassica campestris L. is the important oil-bearing crop in China. Rapeseed cake is the main byproduct of rapeseed oil extraction. As the main active ingredient in rapeseed...     

Effect of Dietary Selenium Supplementation on Growth and Reproduction of Silkworm Bombyx mori L.

Biological Trace Element Research - The effects of selenium (Se) on the growth and reproduction of the Lepidoptera insect, the silkworm, Bombyx mori L were investigated. Initially, the silkworms...     

ROR2 promotes the epithelial-mesenchymal transition by regulating MAPK/p38 signaling pathway in breast cancer

Receptor tyrosine kinase-like orphan receptor 2 (ROR2) is a tyrosine-protein kinase receptor highly implicated in the growth plate and cartilage development, which may be involved in epithelial-mesenchymal transition (EMT) in breast cancer (BC) cells. Although ROR2 is known to promote the migration of BC cells, the detailed mechanism of this event is still not clear. Here, we found that ROR2 expression was significantly increased in BC lymphatic metastatic tissue as well as BC samples compared to normal adjacent breast tissues. A higher expression of ROR2 in MDA-MB-231 and a lower expression of ROR2 in MCF-7 cells were observed. MDA-MB-231-siROR2 cells with ROR2 knockdown inhibited MDA-MB-231 cell invasion, migration, and clonal formation, while MCF-7-OvROR2 cells with overexpression showed the opposite results. The underlying mechanisms involved in ROR2-induced EMT in MDA-MB-231 and MCF-7 cells were further investigated. ROR2 may activate EMT progression in BC cells by altering MAPK kinase 3/6 (MKK3/6) expression. The expressions of transforming growth factor-β, matrix metalloproteinase-2 (MMP-2), and MMP-9, which were related to tumor cell invasion activities, were notably increased in MCF-7-OvROR2 cells. The EMT markers, including snail, N-cadherin, tissue inhibitor of metalloproteinases-1, and vimentin, were significantly upregulated in MCF-7-OvROR2 cells. On the contrary, E-cadherin was obviously reduced expressed in MCF-7-OvROR2 cells. ROR2 may regulate the malignant phenotype of BC cells possibly via activation of mitogen-activated protein kinase (MAPK)/p38 signaling pathway. Collectively, ROR2 promotes BC carcinogenesis by mediating the MAPK/p38 pathway, which is independent of Wnt5α.     

Retracted: LncRNA-LET relieves hypoxia-induced injury in H9c2 cells through regulation of miR-138

Ischemic heart disease (IHD) is a common cardiovascular disease, occurs when coronary artery blood circularity cannot match with the heart's need. The present work attempted to study the effects of long noncoding RNA (lncRNA) low expression in tumor (LET) on the progression of IHD. H9c2 cells were injured by hypoxia to mimic a cell model of IHD. The effects of lncRNA-LET on hypoxia-injured H9c2 cells were tested by using cell counting kit-8 assay, flow cytometry, and Western blot analysis. MicroRNA-138 (miR-138) expression was tested by a quantitative real-time polymerase chain reaction, and the expression of c-Jun N-terminal kinase (JNK) and p38MAPK (p38–mitogen-activated protein kinase) proteins was measured by Western blot analysis. We found that hypoxia exposure significantly repressed the viability of H9c2 cells, and induced apoptosis. Meanwhile, phosphorylation of JNK and p38MAPK was enhanced by hypoxia. The expression of lncRNA-LET was repressed by hypoxia. Overexpression of lncRNA-LET attenuated hypoxia-induced injury in H9c2 cells. Moreover, miR-138 was a downstream effector of lncRNA-LET, that miR-138 was highly expressed in lncRNA-LET-overexpressed cell. The cardioprotective effects of lncRNA-LET were abolished when miR-138 was silenced. In conclusion, this study revealed the cardioprotective function of lncRNA-LET. lncRNA-LET conferred its cardioprotective effects possibly via upregulation of miR-138 and thus repressing the JNK and p38MAPK pathways.     

Circular RNAs expression profiles in plasma exosomes from early-stage lung adenocarcinoma and the potential biomarkers

This study aimed to identify differential circular RNA (circRNA) in the plasma exosomes of patients with lung adenocarcinoma (LUAD) using high-throughput sequencing. First, exosomes were isolated using an exosome isolation kit and confirmed by Western blotting, transmission electron microscopy, and NanoSight Assay. Subsequently, plasma circRNA expression profiles were screened by high-throughput sequencing and confirmed by fluorescence quantitative real-time polymerase chain reaction (qRT-PCR) and Sanger sequencing. Finally, the circRNA-miRNA-mRNA network was performed to forecast the potential function of circRNAs. The result of high-throughput sequencing data documented that 182 differentially expressed exosomal circRNAs in all were screened, which included 105 that were upregulated and 78 that were downregulated in LUAD patients plasma compared with controls. The four upregulated circRNAs including circ_0001492, circ_0001346, circ_0000690, and circ_0001439 were identical to the sequencing data by qRT-PCR, and their latent circRNA-miRNA-mRNA interactions were exhibited. Taken together, our study firstly revealed the altered exosomal circRNA expression from plasma samples in patients with LUAD and supports the need for exploring their potential as biomarkers and the pathological effects of lung cancer.     

SNHG16 as the miRNA let-7b-5p sponge facilitates the G2/M and epithelial-mesenchymal transition by regulating CDC25B and HMGA2 expression in hepatocellular carcinoma

Long noncoding RNAs (lncRNAs) play crucial roles in hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms of small nucleolar RNA host gene 16 (SNHG16) for regulating the cell cycle and epithelial to mesenchymal transition (EMT) remain elusive. In this study, SNHG16 expression profiles of HCC tissues or cell lines were compared with those of normal tissues or hepatocyte cell line. The effect of SNHG16 knockdown in HCC cell lines was investigated by using in vitro loss-of-function experiments and in vivo nude mouse experiments. The potential molecular regulatory mechanism of SNHG16 in HCC progression was investigated by using mechanistic experiments and rescue assays. The results revealed that SNHG16 was highly expressed in HCC tissues and cell lines, which predicted poor prognosis of HCC patients. On one hand, the downregulation of SNHG16 induced G2/M cell cycle arrest, inducing cell apoptosis and suppression of cell proliferation. On the other hand, it inhibited cell metastasis and EMT progression demonstrated by in vitro loss-of-function cell experiments. Besides, knockdown of SNHG16 increased the sensitivity of HCC cells to cisplatin. For the detailed mechanism, SNHG16 was demonstrated to act as a let-7b-5p sponge in HCC. SNHG16 facilitated the G2/M cell cycle transition by directly acting on the let-7b-5p/CDC25B/CDK1 axis, and promoted cell metastasis and EMT progression by regulating the let-7b-5p/HMGA2 axis in HCC. In addition, the mechanism of SNHG16 for regulating HCC cell proliferation and metastasis was further confirmed in vivo by mouse experiments. Furthermore, these results can provide new insights into HCC treatment and its molecular pathogenesis, which may enlighten the further research of the molecular pathogenesis of HCC.