SOX2-induced upregulation of lncRNA LINC01561 promotes non-small-cell lung carcinoma progression by sponging miR-760 to modulate SHCBP1 expression

Long noncoding RNAs (lncRNAs) have been shown to have critical regulatory roles in tumorigenesis. lncRNA LINC01561 (LINC01561) is a newly identified tumor-related lncRNA and its dysregulation has been demonstrated in several tumors. However, whether LINC01561 is involved in the progression of non-small-cell lung carcinoma (NSCLC) and its underlying mechanisms remain unknown. In this study, we first provided evidence that LINC01561 expressions were distinctly upregulated in NSCLC tissues and cell lines. Combining with bioinformatics assays and mechanism experiments, our group demonstrated that LINC01561 was activated by SOX2 in NSCLC. Clinical research revealed that upregulation of LINC01561 was related to poorer clinicopathologic features and shorter survival time. Functionally, suppression of LINC01561 exhibited tumor-suppressive functions through impairing cell proliferation, migration, and invasion as well as inducing apoptosis. Moreover, we verified that LINC01561 could directly bind to miR-760, isolating miR-760 from its target gene SHC SH2 domain-binding protein 1 (SHCBP1). We also found that SHCBP1 was lowly expressed in NSCLC and served as a tumor promoter. A functional study indicated that LINC01561 regulated SHCBP1 expression by competitively binding to miR-760. In summary, our findings indicated that SOX2-induced overexpression of LINC01561 promoted the proliferation and metastasis by acting as a competing endogenous RNA to modulate SHCBP1 by sponging miR-760.     

Induction and maintenance of specific multipotent progenitor stem cells synergistically mediated by Activin A and BMP4 signaling

We recently reported that epiblast stem cells (EpiSCs)-like cells could be derived from preimplantation embryos (named as AFSCs). Here, we established AFSCs from pre-implantation embryos of multiple mouse strains and showed that unlike EpiSCs, the derivation efficiency of AFSCs was affected by the genetic background. We then used AFSCs lines to dissect the roles of Activin A (Act A) and basic fibroblast growth factor and reported that Act A alone was capable of maintaining self-renewal but not developmental potential in vivo. Finally, we established a novel experimental system, in which AFSCs were efficiently converted to multipotent progenitor stem cells using Act A and bone morphogenetic protein 4 (named as ABSCs). Importantly, these ABSCs contributed to neural mesodermal progenitors and lateral plate mesoderm in postimplantation chimeras. Taken together, our study established a robust experimental system for the generation of specific multipotent progenitor stem cells that was self-renewable and capable of contributing to embryonic and extra-embryonic tissues.     

Epigenetic modifier trichostatin A enhanced osteogenic differentiation of mesenchymal stem cells by inhibiting NF-κB (p65) DNA binding and promoted periodontal repair in rats

We wished to evaluate whether epigenetic modifiers have a beneficial effect on treating experimental periodontitis and mechanisms for regulating the cell fate of mesenchymal stem cells (MSCs) in inflammatory microenvironments. We isolated MSCs from healthy and inflamed gingival tissues to investigate whether trichostatin A (TSA) could improve osteogenic differentiation and resolve inflammation in vitro. The tissue regenerative potentials were evaluated when treated with a temperature-dependent, chitosan-scaffold-encapsulated TSA, in a rat model of periodontitis. After induction with the conditioned medium, TSA treatment increased the osteogenic differentiation potential of inflamed MSCs and healthy MSCs. In addition, interleukin-6 and interleukin-8 levels in supernatants were significantly decreased after TSA treatment. Moreover, TSA promoted osteogenic differentiation by inhibiting nuclear factor-κB (p65) DNA binding in MSCs. In rats with experimental periodontitis, 7 weeks after local injections of chitosan-scaffold-encapsulated TSA, histology and microcomputed tomography showed a significant increase in alveolar bone volume and less inflammatory infiltration compared with vehicle-treated rats. The concentrations of interferon-γ and interleukin-6 were significantly decreased in the gingival crevicular fluid after TSA treatment. This study demonstrated that TSA had anti-inflammatory properties and could promote periodontal tissue repair, which indicated that epigenetic modifiers hold promise as a potential therapeutic option for periodontal tissue repair.     

Type locality and species identity of Pareuchiloglanis sinensis (Hora & Silas) with a description of a new species of the genus from the upper Yangtze River basin in southern China

The genus Pareuchiloglanis, distributed in the Salween, Mekong, Red, Pearl and Yangtze River basins in China, Laos, Myanmar and Vietnam, consists of 20 valid species and 5 uncertain species. This study provided a taxonomic revision to Pareuchiloglanis occurring in the Yangtze River. According to the results of a morphological comparison, the type locality of Pareuchiloglanis sinensis was updated to the Nanpan-jiang (the upper Pearl River) basin; five species were identified in Pareuchiloglanis from the Yangtze River basin. Specimens formerly identified as Pareuchiloglanis sinensis from this basin were described as a new species, Pareuchiloglanis chui sp. nov. Moreover, Pareuchiloglanis tianquanensis was synonymized with Pareuchiloglanis sichuanensis. This study provided a key to these two species and three others (Pareuchiloglanis anteanalis, Pareuchiloglanis hupingshanensis and Pareuchiloglanis robusta) from the Yangtze River basin, including information about their geographical distribution. These findings provide an insight into the evolution, distribution and taxonomy of this genus for future studies.     

植物病原真菌的自噬

作为真核生物中普遍存在的现象,自噬不但实现了对细胞内物质的降解和回收利用,而且与植物病原真菌早期侵染阶段的附着胞发育、膨压升高、菌丝体形成、完成侵染等一系列过程密切相关,并且发挥了重要的作用。本文归纳了植物病原真菌自噬的相关基因和自噬过程;总结了自噬对病原真菌生长发育、致病力的调控和影响;概括了病原真菌自噬所涉及的信号通路;阐明了自噬影响植物病原真菌侵染过程的主要分子机制。为今后以自噬相关基因或蛋白作为靶点来筛选抑制病原真菌侵染的新型药物提供新的策略和思路。     

多酶组合催化制备L-高苯丙氨酸

【目的】L-高苯丙氨酸(L-HPA)是许多医药化学品的重要中间体,化学合成法生产L-HPA反应复杂、环境污染严重,本研究旨在开发高效环保的L-HPA酶法合成路线。【方法】采用模块化组装的方法,构建了一条以甘氨酸和苯乙醛为底物高产L-HPA的新途径。【结果】首先,根据文献挖掘设计了一条由苏氨酸醛缩酶(TA)、苏氨酸脱氨酶(TD)、苯丙氨酸脱氢酶(PheDH)和甲酸脱氢酶(FDH)组成的多酶组合催化途径,用于L-HPA的合成。其次,根据氨基基团的引入和重构,将L-HPA多酶组合催化途径分为基础单元和扩增单元,基础单元包括TA和TD,扩增单元包括PheDH和FDH。然后,利用不同表达水平的质粒,对基础单元和扩增单元进行蛋白表达的组合调节,获得最优工程菌BL21-C-M1-R-M2,使L-HPA产量达到208.6mg/L。最后,我们对全细胞转化体系进行优化,使L-HPA产量进一步提高到1226.6 mg/L,苯乙醛摩尔转化率为34.2%。【结论】该工艺路线绿色高效,为未来大规模生产L-HPA奠定基础。