https://scholars.lib.ntu.edu.tw/handle/123456789/481037
標題: | SPANXA suppresses EMT by inhibiting c-JUN/SNAI2 signaling in lung adenocarcinoma | 作者: | Hsiao Y.-J. KANG-YI SU Hsu Y.-C. Chang G.-C. JIN-SHING CHEN Chen H.-Y. Hong Q.-S. Hsu S.-C. Kang P.-H. Hsu C.-Y. Ho B.-C. Yang T.-H. Wang C.-Y. Jou Y.-S. PAN-CHYR YANG SUNG-LIANG YU |
公開日期: | 2016 | 出版社: | Impact Journals LLC | 卷: | 7 | 期: | 28 | 起(迄)頁: | 44417-44429 | 來源出版物: | Oncotarget | 摘要: | SPANXA (Sperm Protein Associated with the Nucleus on the X-chromosome, family members A1/A2) acts as a cancer-testis antigen expressed in normal testes, but dysregulated in various tumors. We found that SPANXA is highly expressed in low-invasive CL1-0 cells compared with isogenous high-invasive CL1-5 cells. SPANXA was preferably expressed in tumor tissues and associated with the prolonged survival of lung adenocarcinomas. SPANXA suppressed the invasion and metastasis of lung cancer cells in vitro and in vivo. By the expression microarray and pathway analysis, we found that the SPANXA-altered genes were enriched in the epithelial- mesenchymal transition (EMT) pathway. SPANXA reduced SNAI2 expression resulted in up-regulating E-cadherin. c-JUN acts as the positive-regulator of EMT. Silencing SPANXA increased c-JUN mRNA expression and blockage of c-JUN led to SNAI2 down-regulation. Our results clearly characterized SPANXA as an EMT inhibitor by suppressing c-JUN-SNAI2 axis in lung adenocarcinoma. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84978722237&doi=10.18632%2foncotarget.10088&partnerID=40&md5=0d829c5a7f2efcaefbeeb2c7cf83bfbf https://scholars.lib.ntu.edu.tw/handle/123456789/481037 |
ISSN: | 1949-2553 | DOI: | 10.18632/oncotarget.10088 | SDG/關鍵字: | beta catenin; cancer testis antigen; nerve cell adhesion molecule; protein c jun; Sperm Protein Associated with the Nucleus on the X chromosome family member A; transcription factor Slug; unclassified drug; uvomorulin; vimentin; nuclear protein; protein c jun; SNAI2 protein, human; SPANXA1 protein, human; transcription factor Snail; animal cell; animal experiment; animal model; animal tissue; Article; cancer survival; cell invasion; cell migration; controlled study; down regulation; E cadherin gene; epithelial mesenchymal transition; gene; gene expression regulation; gene silencing; human; human cell; human tissue; in vitro study; in vivo study; lung adenocarcinoma; lung cancer cell line; metastasis inhibition; mouse; nonhuman; oncogene c jun; overall survival; protein expression; protein function; protein localization; signal transduction; SNAI2 gene; SPANXA gene; upregulation; adenocarcinoma; animal; antagonists and inhibitors; epithelial mesenchymal transition; genetic transfection; genetics; lung tumor; metabolism; pathology; SCID mouse; tumor cell line; xenograft; Adenocarcinoma; Animals; Cell Line, Tumor; Epithelial-Mesenchymal Transition; Heterografts; Humans; Lung Neoplasms; Mice; Mice, SCID; Nuclear Proteins; Proto-Oncogene Proteins c-jun; Signal Transduction; Snail Family Transcription Factors; Transfection; Up-Regulation |
顯示於: | 醫學系 |
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