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Word embedding in the NLP area has attracted increasing attention in recent years. The continuous bag-of-words model (CBOW) and the continuous Skip-gram model (Skip-gram) have been developed to learn distributed representations of words from a large amount of unlabeled text data. In this paper, we explore the idea of integrating extra knowledge to the CBOW and Skip-gram models and applying the new models to biomedical NLP tasks. The main idea is to construct a weighted graph from knowledge bases (KBs) to represent structured relationships among words/concepts. In particular, we propose a GCBOW model and a GSkip-gram model respectively by integrating such a graph into the original CBOW model and Skip-gram model via graph regularization. Our experiments on four general domain standard datasets show encouraging improvements with the new models. Further evaluations on two biomedical NLP tasks (biomedical similarity/relatedness task and biomedical Information Retrieval (IR) task) show that our methods have better performance than baselines.

Dysregulated microRNAs (miRNAs) play crucial roles in the regulation of cancer stem cells (CSCs), and CSCs are closely associated with tumor initiation, metastasis, and recurrence. Here we found that miR-150-5p was significantly downregulated in CSCs of non-small-cell lung cancer (NSCLC) and its expression level was negatively correlated with disease progression and poor survival in patients with NSCLC. Inhibition of miR-150-5p increased the CSC population and sphere formation of NSCLC cells in vitro and stimulated NSCLC cell tumorigenicity and metastatic colonization in vivo. In contrast, miR-150-5p overexpression potently inhibited sphere-formed NSCLC cell tumor formation, metastatic colonization, and recurrence in xenograft models. Furthermore, we identified that miR-150-5p significantly inhibited wingless (Wnt)-beta-catenin signaling by simultaneously targeting glycogen synthase kinase 3 beta interacting protein (GSKIP) and beta-catenin in NSCLC cells. miR-150-5p also targeted high mobility group AT-hook 2 (HMGA2), another regulator of CSCs, and Wnt-beta-catenin signaling. The restoration of HMGA2 and beta-catenin blocked miR-150-5p overexpression-induced inhibition of CSC traits in NSCLC cells. These findings suggest that miR-150-5p functions as a CSC suppressor and that overexpression of miR-150-5p may be a novel strategy to inhibit CSC-induced metastasis and recurrence in NSCLC.