No abstract

Silicon (Si) is generally considered a beneficial element for the growth of higher plants, especially for those grown under stressed environments. Recently, the mitigating role of Si in cadmium (Cd) stress has received some attention. However, its mechanisms involved remain poorly understood. We studied the effects of Si on tissue and subcellular distribution of Cd, as well as the activities of major antioxidant enzymes (SOD, POD and CAT) with two contrasting peanut (Arachis hypogaea L.) cultivars (Luhua 11 and Luzi 101) differing in their Cd tolerance. The results showed that Cd exposure alone depressed plant growth and caused oxidative stress for both cultivars, and this toxicity was more obvious in Cd-sensitive cultivar (Luhua 11) than in Cd-tolerant cultivar (Luzi 101). Si supply significantly alleviated the toxicity of Cd in peanut seedlings; this was correlated with a reduction of shoot Cd accumulation, an alteration of Cd subcellular distribution in leaves, and a stimulation of antioxidative enzymes. The mechanisms of Si amelioration of Cd stress were cultivar and tissue dependent. For Luhua 11, Si-mediated inhibition of Cd transport from roots to shoots, reduction of Cd content in cell organelle fractions of leaves, and enhancement of the SOD, POD and CAT activities in roots, might responsible for the role of Si in alleviating Cd toxicity. For Luzi 101, Si alleviation of Cd toxicity is mainly attributed to the decrease in Cd concentration in shoot and stimulation of antioxidants systems.

Signal Transducer and Activator of Transcription 3 (STAT3), a common oncogenic mediator, is constitutively activated in many types of human cancers; therefore it is a major focus in the development of novel anti-cancer agents. Hedyotis diffusa Willd has been used as a major component in several Chinese medicine formulas for the clinical treatment of colorectal cancer (CRC). However, the precise mechanism of its anti-tumor activity remains largely unclear. Using a CRC mouse xenograft model, in the present study we evaluated the effect of the ethanol extract of Hedyotis diffusa Willd (EEHDW) on tumor growth in vivo and investigated the underlying molecular mechanisms. We found that EEHDW reduced tumor volume and tumor weight, but had no effect on body weight gain in CRC mice, demonstrating that EEHDW can inhibit CRC growth in vivo without apparent adverse effect. In addition, EEHDW treatment suppressed STAT3 phosphorylation in tumor tissues, which in turn resulted in the promotion of cancer cell apoptosis and inhibition of proliferation. Moreover, EEHDW treatment altered the expression pattern of several important target genes of the STAT3 signaling pathway, i.e., decreased expression of Cyclin D1, CDK4 and Bcl-2 as well as up-regulated p21 and Bax. These results suggest that suppression of the STAT3 pathway might be one of the mechanisms by which EEHDW treats colorectal cancer.

To assess the role of salicylic acid (SA) in alleviating cadmium (Cd) toxicity in hemp (Cannabis sativa L.) plants, the growth parameters, Cd accumulation, photosynthetic performance and activities of major antioxidant enzymes were investigated in hemp seedlings treated with 500 lM SA, under 0, 25, 50, and 100 mg Cd kg -1 sands (DW) conditions, respectively. Cd exposure resulted in a small reduction in biomass (12.0-26.9% for root, and 8.7-29.4% for shoot, respectively), indicating hemp plants have innate capacity to tolerant Cd stress. This was illustrated by little inhibition in photosynthetic performance, unchanged malondialdehyde content, and enhancement of superoxide dismutase (SOD) and peroxidases (POD) activities in hemp plants. Cd content in root is 25.0-29.5 times' higher than that in shoot, suggesting the plant can be classified as a Cd excluder. It is concluded that SA pretreatment counteracted the Cd-induced inhibition in plant growth. The beneficial effects of SA in alleviating Cd toxicity can be attributed to the SA-induced reduction of Cd uptake, improvement of photosynthetic capacity, and enhancement of SOD and POD activities.

Genetic mapping with RAPD markers has been initiated in Citrus. Reproducible polymorphism of amplified DNA fragments was obtained with approximately half of the 140 random primers tested, revealing 266 segregating loci. These were tested for linkage using 60 BC1 progeny from an intergeneric cross of Citrus grandis (L.) Osb. x [Citrus grandis (L.) Osb. x Poncirus trifoliata (L.) Raf.]. A core linkage map was constructed that consists of nine linkage groups containing 109 RAPD markers and 51 previously-mapped RFLP and isozyme markers. A further 79 markers that could not be ordered unambiguously because of their allelic constitution were associated with individual linkage groups and are shown in relation to the core map. The core map has a total length of 1192 cM with an average distance of 7.5 cM between loci and is estimated to cover 70-80% of the genome. Loci with distorted segregation patterns clustered on several linkage groups. Individual clusters of loci were skewed in allelic composition toward one or the other parent, usually C. grandis. This relatively-saturated linkage map will eventually be used to identify quantitative trait loci for cold and salt-tolerance in Citrus. As a beginning we have mapped three loci detected by a cold-acclimation-responsive cDNA.

No abstract

The stable differentiation in rDNA FISH pattern between the subgenera suggests that chromosomal rearrangements played a role in the splitting of the two subgenera, and transpositional events rather than major structural changes are likely responsible for the variable rDNA distribution patterns among species of the same subgenus with conserved karyotypes.

Abstract. Signal transducer and activator of transcription 3 (STAT3) is persistently activated in cancer cells and contributes to malignant progression in various types of cancer. The Janus-activated kinase (JAK) family phosphorylates STAT3 in response to stimulation by cytokines or growth factors. The JAK1-STAT3 signaling pathway plays an important role in cell proliferation and apoptosis. Nitidine chloride (NC) is a benzophenanthridine alkaloid that has been reported as an antitumor agent due to its its inhibitory effects on topoisomerase I. Using a mouse xenograft model of hepatocellular carcinoma (HCC), this study aimed to evaluate the effects of NC on tumor growth in vivo and to elucidate the underlying mechanisms. The analysis of the effects of NC on apoptosis in HCC tumor xenografts in mice was carried out by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expression of Bcl-2, Bax, cyclin-dependent kinase (CDK)4, cyclin D1, p21 and proliferating cell nuclear antigen (PCNA) was analyzed by immunohistochemistry; and the protein expression of JAK1 and STAT3 was examined by western blot analysis. Our results revealed that treatment with NC decreased the tumor volume and tumor weight, suggesting that NC inhibits HCC cell growth in vivo. In addition, NC blocked the activation of JAK1-STAT3 in the tumor tissues, which in turn resulted in the induction of cancer cell apoptosis and the inhibition of proliferation. Consequently, treatment with NC downregulated the expression of cyclin D1, CDK4 and Bcl-2 and increased the level of p21 and Bax. Our data provide a molecular basis for the antitumor activity of NC. IntroductionHepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality worldwide (1,2) and it has been reported that more than 600,000 individuals succumb to the disease each year (1). It is the second most common cause of cancer-related mortality in China, and 75% of known new cases and deaths in the Asia-Pacific region (3-5). Currently, the main treatment methods for liver cancer include surgical resection, radiotherapy and chemotherapy (4,6). Although surgical resection (which involves removing the tumor completely) offers the best prognosis for long-term survival, only 10-15% of patients are suitable for surgical resection, as the tumor may be too large, or may have grown into major blood vessels or other vital organs (7-9). Related data demonstrate that the percentage of HCC cells is already high at diagnosis with a high expression of the multidrug resistance gene and conventional chemotherapy of HCC fails to provide satisfactory remission and may cause serious side-effects (6,10). Thus, it is necessary to develop a novel effective drug for the treatment of HCC. Natural products have attracted much attention in the search for novel anticancer therapeutic agents as they have relatively few side-effects and have long been used as alternative therapies for various diseases, including cancer (11,12). Therefore, determining naturally occurrin...