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  • mitoxantrone and In the present study promoting bile acid sy

    2019-10-08

    In the present study, promoting bile mitoxantrone and synthesis by activating EP4 receptors was shown to exert protection against hepatic steatosis. This finding may be relevant for treatment of non-alcoholic fatty liver disease, a major cause of liver disease and prominent indication for liver transplantation in the Western world [41]. Although many therapeutic compounds are under active investigation in clinical trials [41], there are currently no unequivocally effective medical treatment options for non-alcoholic fatty liver other than weight loss. The following are the supplementary data related to this article.
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    Introduction Lung cancer, especially non-small cell lung cancer (NSCLC), is the most lethal malignancy in the world, with the highest mortality and poor survival (Siegel et al., 2017). Despite advancement in management, the outcomes are still unfavorable. Tobacco smoke, adverse environmental factors, genetic contributions, and the presence of chronic lung diseases such as chronic obstructive pulmonary disease (COPD) are the main factors that account for the occurrence and development of this illness (Hong et al., 2015). A large body of evidence have shown that traditional Chinese medicine (TCM) including Chinese herbal medicine (CHM) can be beneficial for the treatment of advanced cancers with low-toxic effects. TCM remedies can improve the quality of life, reduce symptom distress, and increase physical function when used in combination with other treatments for patients with cancer including advanced NSCLC (Jiang et al., 2016; Li et al., 2013; Tang et al., 2016; Ting et al., 2017; Zhang et al., 2018, 2019), suggesting the benefit of adjuvant therapeutic alternatives in these patients. Xiaoji Decoction (XJD) has been used in the treatments of lung cancer for many years (Chai et al., 2014) and mechanistically has been shown to inhibit the growth of NSCLC cells in vitro and in vivo (Chai et al., 2014). However, the mechanistic details of the potential therapeutic benefits of XJD for patients with lung cancer have not been well described. We previously observed that XJD inhibited proliferation of NSCLC cells via AMP-activated protein kinase alpha (AMPKα)-mediated inhibition of transcription factor SP1 protein levels followed by suppressing DNA methyltransferase 1 (DNMT1) expression both in vitro and in vivo (Zhao et al., 2016). However, multiple compounds and complicated metabolic processes of XJD may affect a variety of pathways and interactions of potential targets. Thus, the underlying molecular mechanisms associated with the therapeutic potential of XJD, including its action to sensitize the effect of gefitinib on cancer have not been fully elucidated. Long noncoding RNAs (lncRNAs) are transcripts >200 nucleotides with no protein-coding potential and play important roles in cancer biology. Of the characterized lncRNAs, the HOX transcript antisense intergenic RNA (HOTAIR), an approximately 2.2 kb long noncoding RNA transcribed from the HOXC locus, is regarded as an oncogene, and can reprogram chromatin organization and promote tumor progression (Botti et al., 2017). Overexpression of HOTAIR has been observed in several types of human cancers and is linked to tumor invasion, progression, metastasis, and poor prognosis through multiple signaling mechanisms. The important role of HOTAIR in cancer biology has stimulated interest in HOTAIR as a potential therapeutic target (Loewen et al., 2014; Lu et al., 2017; Malek et al., 2014; Wu et al., 2014). HOTAIR can mediate a physical interaction between Snail, a transcription factor and a master regulator of epithelial-to-mesenchymal transition (EMT), and enhancer of zeste homolog 2 (EZH2), an enzymatic subunit of the polycomb-repressive complex 2. HOTAIR is a crucial player in Snail-mediated EMT in epithelial and hepatic morphogenesis (Battistelli et al., 2017). In addition, HOTAIR has been explored as a biomarker in lung cancer because its elevated expression is correlated with metastasis, drug resistance, and poor survival in patients with lung cancer (Loewen et al., 2014). Nevertheless, the potential impact of this lncRNA on the occurrence, growth, and progression of lung malignancy still remain to be determined.