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Xiaoxiao Xue,1 Yatao Guo,2 Qianying Zhao,3 Yongwen Li,1 Mi Rao,1 Wenjing Qi,1 Huijuan Shi1 1Department of Dermatovenereology, the General Hospital of Ningxia Medical University, Yinchuan, 750004, People’s Republic of China; 2Dermatological Department, Baoji Central Hospital, Shaanxi, 721008, People’s Republic of China; 3Medical Experimental Center, the General Hospital of Ningxia Medical University, Yinchuan, 750004, People’s Republic of ChinaCorrespondence: Huijuan Shi, Department of Dermatovenereology, the General Hospital of Ningxia Medical University, Yinchuan, 750004, People’s Republic of China, Tel +86-13995295912, Email shjyjm@163.comPurpose: Psoriasis is a common, chronic, inflammatory, recurrent, immune-mediated skin disease. Oxymatrine is effective for treating moderate and severe psoriasis. Here, transcriptional changes in skin lesions before and after oxymatrine treatment of patients with psoriasis were identified using full-length transcriptome analysis and then compared with those of normal skin tissues.Patients and Methods: Co-expression modules were constructed by combining the psoriasis area and severity index (PASI) score with weighted gene co-expression network analysis to explore the action mechanism of oxymatrine in improving clinical PASI. The expression of selected genes was verified using immunohistochemistry, quantitative real-time PCR, and Western blotting.Results: Kyoto Encyclopedia of Gene and Genome pathway analysis revealed that oxymatrine treatment reversed the abnormal pathways, with an improvement in lesions and a reduction in PASI scores. Gene Ontology (GO) analysis revealed that oxymatrine treatment led to altered GO terms being regulated with a decrease in the PASI score in patients. Therefore, oxymatrine treatment may improve the skin barrier, differentiation of keratinocytes, and alleviate abnormality of organelles such as desmosomes. Protein-protein interaction network interaction analysis revealed that the top five hub

Min Gao,1,2,&ast; Yongwen Li,3,&ast; Hua Huang,4,&ast; Yaguang Fan,3 Ruifeng Shi,4 Lianchun Su,5 Chen Chen,3 Xuanguang Li,4 Guangsheng Zhu,4 Di Wu,4 Peijun Cao,4 Hongyu Liu,3 Jun Chen,3– 5 Shirong Kang1 1Department of Thoracic Surgery, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot, 010010, People’s Republic of China; 2Inner Mongolia Medical University, Hohhot, 010010, People’s Republic of China; 3Tianjin Key Laboratory of Lung Cancer Metastasis and Tumor Microenvironment, Tianjin Lung Cancer Institute, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 4Department of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin, 300052, People’s Republic of China; 5Department of Thoracic Surgery, First Affiliated Hospital of Shihezi University School of Medicine, Shihezi, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Jun Chen; Shirong Kang, Email huntercj2004@qq.com; bssbzzk2013@163.comBackground: Genetic susceptibilities play a large role in the pathogenesis of lung cancer (LC). The polycomb repressive complex 2 (PRC2) is a conserved chromatin-associated complex that represses gene expression and is crucial for proper organismal development and gene expression patterns. Despite PRC2 dysregulation has been observed in various human cancers, the relationship between PRC2 genes variants and lung cancer risk remains largely unexplored.Methods: To investigate the association between single nucleotide polymorphisms (SNPs) in PRC2 genes and the risk of developing LC, we genotyped blood genomic DNA from 270 LC patients and 452 healthy individuals of Chinese Han ethnicity using the TaqMan™ genotyping technique.Results: We found that rs17171119T>G(adjusted odds ratio (OR) = 0.662, 95% CI: 0.467– 0.938, P < 0.05), rs10898459 T>C(adjusted OR = 0.615, 95% CI: 0.4– 0.947, P < 0.05), and rs1136258 C>T(adjusted OR = 0.273

Guanghui Xie,1,2,* Yongwen Li,1,* Yongjun Jiang,2,* Xian Ye,2 Jianfeng Tang,2 Jun Chen1 1Department of Lung Cancer Surgery, Tianjin Medical University General Hospital, Tianjin, People’s Republic of China; 2Department of Cardiothoracic Vascular Surgery, The Central Hospital of Yongzhou, Yongzhou, Hunan Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jun ChenDepartment of Lung Cancer Surgery, Tianjin Medical University General Hospital, No. 154 Anshan Road, Heping District, Tianjin, 300052, People’s Republic of ChinaEmail huntercj2004@yahoo.comIntroduction: Non-small cell lung cancer (NSCLC) is the most common form of lung cancer, accounting for approximately 80%– 85% of all cases of lung cancer. Huntingtin interacting protein-1 interacting protein (HIPPI) is a transcription regulator and plays an important role in apoptotic cell death. However, the role of HIPPI in NSCLC remains unclear.Methods: Immunohistochemistry (IHC) and qRT-PCR were performed for expression analysis. The roles of HIPPI were studied using cell counting kit-8 (CCK-8), colony formation, flow cytometry, wound healing, Transwell invasion assays and mouse xenograft model. Gene microarray analysis and bioinformatics analysis were used to identify differentially expressed genes after HIPPI silencing.Results: HIPPI is highly expressed in NSCLC tissues relative to adjacent normal tissues. Targeting HIPPI by RNA interference inhibits NSCLC cell proliferation in vitro and tumor growth in vivo. HIPPI silencing also attenuates cell migration and invasion and enhances cisplatin sensitivity in NSCLC cells. Mechanistic investigation suggests that HIPPI can positively regulate the expression of MCM2, MCM6 and MCM8, which are key regulators of DNA replication. Furthermore, consistent with HIPPI, MCM2, MCM6 and MCM8 are also upregulated in NSCLC tissues.Conclusion: Our study highlights the importance of HIPPI for tumor biol