Bioinformatic Tools for the Analysis and Prediction of ncRNA Interactions

Noncoding RNAs (ncRNAs) play prominent roles in the regulation of gene expression via their interactions with other biological molecules such as proteins and nucleic acids. Although much of our knowledge about how these ncRNAs operate in different biological processes has been obtained from experimental findings, computational biology can also clearly substantially boost this knowledge by suggesting possible novel interactions of these ncRNAs with other molecules. Computational predictions are thus used as an alternative source of new insights through a process of mutual enrichment because the information obtained through experiments continuously feeds through into computational methods. The results of these predictions in turn shed light on possible interactions that are subsequently validated experimentally. This review describes the latest advances in databases, bioinformatic tools, and new in silico strategies that allow the establishment or prediction of biological interactions of ncRNAs, particularly miRNAs and lncRNAs. The ncRNA species described in this work have a special emphasis on those found in humans, but information on ncRNA of other species is also included.     

多特征融合的lncRNA识别与其功能预测

针对传统的基于单一特征的植物lncRNA识别的局限性,提出了融合RNA序列的开放阅读框、二级结构以及k-mers等多特征方法,训练高斯朴素贝叶斯、支持向量机和梯度提升决策树3种经典的分类模型,并实现分类结果的集成,利用交叉验证对模型的性能进行了评估,整体性能优于目前较流行的CPAT、CNCI和PLEK预测软件,在拟南芥数据集上总体的准确率达到了89%。另外,基于内源性竞争规则以及RNA结构信息,分别对lncRNA-microRNA和microRNA-mRNA进行靶向预测、筛选,再通过整合预测数据建立互作网络,并对网络模块中的lncRNA进行功能预测。通过GO术语分析,对与mRNA相关的lncRNA可能参与的生物调控过程进行预测,推测它们的相应功能。     

lncRNA与Wnt/β-catenin通路的相互关系在结直肠癌中的研究进展

结直肠癌是全球高发病率高死亡率的恶性肿瘤之一，其发病机制研究一直受到国内外的高度关注。长链非编码RNA(long non-coding RNA，lncRNAs) 是一类长度大于200 个核苷酸但无蛋白编码功能的RNA。近期的研究显示lncRNA可通过参与细胞信号转导，并影响信号通路中相关分子的表达，对肿瘤的发生发展产生促进或抑制作用。其中lncRNA与Wnt/β-catenin信号通路的相互调节作用与结直肠癌的发生发展关系密切，lncRNA或Wnt/β-catenin信号通路中相关分子的变化均会影响结直肠癌的增殖、侵袭迁移及耐药。深入了解lncRNA与Wnt/β-catenin信号通路的相互调节作用，可以进一步阐明结直肠癌的发病机制，为结直肠癌的个体化治疗提供新的治疗靶点。     

促进质量提升的课堂教学评价改革

对教学质量的理解是实施课堂教学评价的认识前提,进行课堂教学评价改革则是促进教学质量提升的重要手段。在质量提升要求下,受破除"五唯"评价痼疾的社会需求和教学质量内涵影响,课堂教学评价表现出了多元指标衡量、教学活动全面评价和重视主体素养评价的诉求。但在"唯分数"评价导向下,课堂教学评价却面临着侧重标准划一的量化评价、失落师生主体对非智力因素的价值判断和偏离育人导向的发展旨趣等困境。因此,应通过教学质量的理念诠释导引课堂教学评价改革合理定位,并从师生评价主体承责、"量质"评价方法统整和育人评价环境创设等方面改革课堂教学评价,以促进教学质量提升。     

PRKAR1B-AS2 Long Noncoding RNA Promotes Tumorigenesis,Survival, and Chemoresistance via the PI3K/AKT/mTOR Pathway

Many long noncoding RNAs have been implicated in tumorigenesis and chemoresistance; however, the underlying mechanisms are not well understood. We investigated the role of PRKAR1B-AS2 long noncoding RNA in ovarian cancer (OC) and chemoresistance and identified potential downstream molecular circuitry underlying its action. Analysis of The Cancer Genome Atlas OC dataset, in vitro experiments, proteomic analysis, and a xenograft OC mouse model were implemented. Our findings indicated that overexpression of PRKAR1B-AS2 is negatively correlated with overall survival in OC patients. Furthermore, PRKAR1B-AS2 knockdown-attenuated proliferation, migration, and invasion of OC cells and ameliorated cisplatin and alpelisib resistance in vitro. In proteomic analysis, silencing PRKAR1B-AS2 markedly inhibited protein expression of PI3K-110α and abrogated the phosphorylation of PDK1, AKT, and mTOR, with no significant effect on PTEN. The RNA immunoprecipitation detected a physical interaction between PRKAR1B-AS2 and PI3K-110α. Moreover, PRKAR1B-AS2 knockdown by systemic administration of 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine nanoparticles loaded with PRKAR1B-AS2–specific small interfering RNA enhanced cisplatin sensitivity in a xenograft OC mouse model. In conclusion, PRKAR1B-AS2 promotes tumor growth and confers chemoresistance by modulating the PI3K/AKT/mTOR pathway. Thus, targeting PRKAR1B-AS2 may represent a novel therapeutic approach for the treatment of OC patients.