SPANXA suppresses EMT by inhibiting c-JUN/SNAI2 signaling in lung adenocarcinoma

Yi Jing Hsiao, Kang Yi Su, Yi Chiung Hsu, Gee Chen Chang, Jin Shing Chen, Hsuan Yu Chen, Qi Sheng Hong, Shih Chun Hsu, Po Hsiang Kang, Chia Ying Hsu, Bing Ching Ho, Tsung Hui Yang, Chia Yu Wang, Yuh Shan Jou, Pan Chyr Yang, Sung Liang Yu

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

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.

Original languageEnglish
Pages (from-to)44417-44429
Number of pages13
JournalOncotarget
Volume7
Issue number28
DOIs
StatePublished - 2016

Keywords

  • AP-1
  • E-cadherin
  • Metastasis
  • SLUG
  • SPANX family

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