Reversible acetylation of Lin28 mediated by PCAF and SIRT1.

Lin28 is a small RNA-binding protein that plays an important role in regulating developmental timing, stem cell reprogramming, and oncogenesis. However, the significance of the effect of post-translational modifications on Lin28 activity is not fully understood. In this study, we demonstrated that PCAF directly interacted with and acetylated Lin28. We also showed that the acetylation of Lin28 can be specifically reversed by the deacetylase SIRT1. These findings suggest that the PCAF/SIRT1 balance plays an important role in regulating Lin28 activity. Furthermore, we found that the cold shock domain of Lin28 is the major target of PCAF-mediated acetylation, which leads to a severe reduction in the Lin28 protein levels and an increase in the level of mature let-7a. This study provides the first demonstration that post-translational modification regulates Lin28 activity during let-7a biogenesis and sheds light on the regulation of Lin28 in ES cells and carcinogenesis.

A comprehensive evaluation of circ_0065214/ miR-188-3p/GPNMB axis in breast cancer.

CircRNAs are involved in multiple aspects during carcinogenesis, including tumorigenesis, vascularization, apoptosis and others. Exploring the role of circRNAs in breast cancer (BC) enables us to understand the development mechanism of BC more comprehensively. Here, we screened out and verified an up-regulated circRNA in BC from GEO data. Quantitative Real-time PCR (qRT-PCR) showed that circ_0065214 had a high expression level in BC patients. Besides, circ_0065214 had good diagnostic value in BC serum, and the area under the diagnostic curve, sensitivity and specificity were 0.78, 0.63 and 0.85, respectively. The combined application of circ_0065214 with CEA and CA-153 can further improve the diagnostic efficiency. The knockdown of circ_0065214 in vivo and in vitro inhibited the proliferation, migration and invasion of BC, but promoted autophagy. At last, dual-luciferase reporter assay and rescue assays revealed that circ_0065214 acted as a decoy to adsorb miR-188-3p, and then relieved the repressive effect of miR-188-3p on its target GPNMB. Our results demonstrated that circ_0065214 regulated the expression of GPNMB by competitively binding to miR-188-3p, thus promoting the proliferation, migration and invasion of breast cancer cells and inhibiting autophagy. These findings provided an original therapeutic strategy for BC.

Exosomal miR-1910-3p promotes proliferation, metastasis, and autophagy of breast cancer cells by targeting MTMR3 and activating the NF-κB signaling pathway.

Exosomes are key mediators of intercellular communication and play a role in the pathogenesis and progression of cancer. Exosomes in circulating body fluids serve as molecular markers for cancer diagnosis. This study aimed to investigate the role of exosomal microRNA (miR)-1910-3p in breast cancer and determine its clinical diagnostic value. MiR-1910-3p promoted proliferation and migration of breast cancer cells in vitro and in vivo. In vitro, exosomes enriched in miR-1910-3p transferred miR-1910-3p to mammary epithelial cells and breast cancer cells, promoting proliferation and migration, inhibiting apoptosis, and inducing autophagy. In vivo, exosomes enriched in miR-1910-3p promoted the proliferation and migration of breast cancer cells. MiR-1910-3p downregulated myotubularin-related protein 3, activated the NF-κB and wnt/ß-catenin signaling pathway, and promoted breast cancer progression. Serum miR-1910-3p in exosomes was an effective diagnostic marker that improved the sensitivity of breast cancer diagnosis when used in combination with the traditional tumor marker CA153. In conclusion, breast cancer cell-derived exosomes promoted the growth, metastasis, and autophagy of breast cancer cells by transferring miR-1910-3p. MiR-1910-3p in serum exosomes may serve as a novel molecular marker for breast cancer diagnosis.

[Identification of genes related to resistance to Magnaporthe grisea using differential display technique in rice].

Rice blast caused by Magnaporthe grisea is one of the most serious constraints on high productivity. Understanding the mechanism of the infection of Magnaporthe grisea and the change of gene expression after infection is useful to control blast disease in rice. This work presents the isolation of differentially expressed cDNA fragments from rice leaf induced by the inoculum suspension of Magnaporthe grisea using mRNA differential display technique. Total 87 differential expressed cDNA fragments were recoveried and reamplified. The dot-blotting results showed that 6 fragments of 81 were confirmed to be the expression induced by Magnaporthe grisea inoculum. Those fragments were then cloned into vectors for sequencing. Sequence analysis through Internet Blast searching showed that 3 fragments were novel gene fragments. One was homologous with a putative malate synthase gene on rice chromosome 4 with 78% identities of amino acid; one was highly homologous (75% identity) with rice RPR1 gene on chromosome 11, which has a conservative structure of NBS-LRR domain and may be related to signal transduction of rice defense reaction;another one was homologous with a putative thioredoxin gene on rice chromosome 6 with the identity of 72%.

[Molecular mapping of quantitative trait loci (QTL) for characters of vascular bundles in peduncle related to indica-japonica differentiation in rice (Oryza sativa L.)].

A doubled-haploid population, consisting of 81 DH lines derived from the F1 hybrid of a cross between an indica cultivar and a japonica cultivar, was used to map quantitative trait loci (QTL) controlling numbers of vascular bundles in peduncle, primary rachis branches and the ratio of vascular bundles to primary rachis branches (V/R ratio). For vascular bundles, three QTL were detected. Among them, the QTL qVB-8 with the largest effect individually accounted for 31.1% of the total variation. Two QTL controlling primary rachis branches were identified and they were co-located with 2 of the 3 QTL for vascular bundles respectively. Three QTL for the V/R ratio were mapped on chromosome 1, 2 and 8, respectively. Of the three QTL, the QTL qV/R-1 with the largest additive effect, explained 25.3% of the total variation, was located on chromosome 1 and found to be closely linked to the gene sh-2, a major gene underlying grain-shattering ability. In addition, four and two pairs of significant epistatic QTL were detected for vascular bundles and the V/R ratio, respectively, but none for rachis branches. Our results suggested that the numbers of vascular bundles and primary rachis branches were independently controlled by different polygenic systems, but the two polygenic systems shared a fraction of quantitative trait loci. It was also shown that the chromosome region carrying the QTL qV/R-1 on chromosome 1 might play an important role in the processes of indica-japonica differentiation in rice.

[Study on transgenic elite indica container line D297B containing foreign insect-resistant gene gna].

It was reported in this article that the transgenic elite indica container line D297B containing snowdrop lectin (Galanthus nivalis agglutinin, GNA) gene gna was obtained by biolisties. PCR, Southern blotting and Western blotting indicated that the transgenes were integrated into the genome of D297B and expressed in transgenic plants. Analysis of protein activity showed that product of transgene had activity of agglutinin. Resistance of transgenic seeds to Hygromycin B suggested that the transgenes were integrated in a single locus and inherited according to the pattern of 3:1 in most of transgenic plants. In addition, the PCR analysis revealed that the insect-resistant gene gna and selective marker gene hpt were co-integrated and co-inherited.