Abstract:
:SALL4, a zinc-finger transcriptional factor for embryonic stem cell self-renewal and pluripotency, has been suggested to be involved in tumorigenesis. The role of SALL4 in human gastric cancer, however, remains largely unknown. In this study, we demonstrated that SALL4 was aberrantly expressed at both mRNA and protein levels in human gastric cancer tissues, and SALL4 level was highly correlated with lymph node metastasis. Enforced expression of SALL4 enhanced the proliferation and migration of human gastric cancer cells, whereas knockdown of SALL4 by siRNA led to the opposite effects. In addition, SALL4 overexpression promoted the growth and metastasis of gastric xenograft tumor in vivo. SALL4 overexpression induced epithelial-mesenchymal transition (EMT) in gastric cancer cells, with increased expression of Twist1, N-cadherin and decreased expression of E-cadherin. Moreover, SALL4 promoted the acquirement of stemness in gastric cancer cells through the induction of Bmi-1 and Lin28B. Taken together, our findings indicate that SALL4 has oncogenic roles in gastric cancer through the modulation of EMT and cell stemness, suggesting SALL4 as a novel target for human gastric cancer diagnosis and therapy.
journal_name
Oncogenejournal_title
Oncogeneauthors
Zhang L,Xu Z,Xu X,Zhang B,Wu H,Wang M,Zhang X,Yang T,Cai J,Yan Y,Mao F,Zhu W,Shao Q,Qian H,Xu Wdoi
10.1038/onc.2013.495subject
Has Abstractpub_date
2014-11-27 00:00:00pages
5491-500issue
48eissn
0950-9232issn
1476-5594pii
onc2013495journal_volume
33pub_type
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