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Jie Cheng,Jingxiang Chen,Tong Lin 한국응용곤충학회 2017 Journal of Asia-Pacific Entomology Vol.20 No.4
Heortia vitessoides Moore, a defoliating pest in Aquilaria sinensis (Loureiro) Sprenger forests, is responsible for significant damage to the trees. There is a lack of nucleotide and protein sequence information for H. vitessoides. Hence, in this study, the transcriptome of H. vitessoides was sequenced using the Illumina Hiseq 2000 platform to evaluate the expression profiles and predict the functional genes. A total of 60,587,900 clean reads were produced and de novo assembled into 66,673 unigenes of average length 957 bp; 28,202 and 27,339 identified unigenes were annotated using the National Center for Biotechnology Information (NCBI) non-redundant (NR) database and Swiss-Prot database, respectively. All assembled unigenes were categorized into 64 biological processes, cellular components, or molecular functions using Gene Ontology (GO). In total, 24,278 unigenes were annotated using a database of eukaryotic orthologous groups (KOG) and assigned to 25 functional categories. Of these, 9172 unigenes had matches in the Kyoto Encyclopedia of Genes and Genomes (KEGG) and were assigned to 344 KEGG pathways. In addition, there were 11,670 simple sequence repeats (SSRs) in 66,673 unigenes and 64 repeated motif types, of which A/T was the most frequent. We also found that 1000 unigenes were related to insecticide resistance. To the best of our knowledge, this is the first comprehensive transcriptome analysis for H. vitessoides, providing valuable genome data sources for the study of the molecular biology of this pest
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FNC inhibits non-small cell lung cancer by activating the mitochondrial apoptosis pathway
Jing Xiang,Niu Shuai,Liang Yi,Chen Huiping,Wang Ning,Peng Youmei,Ma Fang,Yue Wanying,Wang Qingduan,Chang Junbiao,Zhang Yi,Zhang Yan 한국유전학회 2022 Genes & Genomics Vol.44 No.1
Background: Previously, we published that 4'-azid-2'-deoxy-2'-fluorarabinoside (FNC), a novel cytosine nucleoside analog, has good anti-viral and anti-tumor activity. Objective: This study aimed to further explore the role and molecular mechanism of FNC in non-small cell lung cancer (NSCLC). Methods: FNC was tested in the NSCLC H460 cell line, the Lewis mouse model, and the H460 cell xenograft model. The effects of FNC were assessed by cell viability, transwell migration, and wound scratch analyses of cell migration and invasion. Apoptosis was assessed by flow cytometry. Proteins expression was assessed by western blot and immunohistochemistry staining (IHC). Results: FNC inhibits the proliferation and metastasis of H460 cells in a time- and dose-dependent manner. FNC treatment showed efficacy and low toxicity in the Lewis mouse lung cancer model as well as in the H460 cell xenograft model. Further, FNC induced H460 cell apoptosis through the activation of the mitochondrial pathway. Notably, FNC inhibited invasion by increasing E-cadherin protein and reducing the protein expression of VEGF, MMP-2, MMP-9, and CD31. Conclusion: FNC inhibits NSCLC by activating the mitochondrial apoptosis pathway and regulating the expressions of multiple proteins related to cell adhesion and invasion, highlighting its potential as an NSCLC therapeutic.
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