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10.18632/oncotarget.13559

http://scihub22266oqcxt.onion/10.18632/oncotarget.13559
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C5349956!5349956!27894099
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suck abstract from ncbi


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pmid27894099      Oncotarget 2016 ; 7 (52): 86816-28
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  • Peroxiredoxin 2 is essential for maintaining cancer stem cell-like phenotype through activation of Hedgehog signaling pathway in colon cancer #MMPMID27894099
  • Wang R; Wei J; Zhang S; Wu X; Guo J; Liu M; Du K; Xu J; Peng L; Lv Z; You W; Xiong Y; Fu Z
  • Oncotarget 2016[Dec]; 7 (52): 86816-28 PMID27894099show ga
  • Cancer stem cells (CSCs) are a key target for reducing tumor growth, metastasis, and recurrence. Redox status is a critical factor in the maintenance of CSCs, and the antioxidant enzyme Peroxiredoxin 2 (Prdx2) plays an important role in the development of colon cancer. Therefore, we investigated the contribution of Prdx2 to the maintenance of stemness of colon CSCs. Here, we used short-hairpin RNAs and a Prdx2-overexpression vector to determine the effects of Prdx2. We demonstrated that knockdown of Prdx2 reduced the self-renewal and sphere formation and resulted in increased 5-FU-induced apoptosis in human colon CSCs. Prdx2 overexpression induced reversion of the self-renewal and sphere formation. Furthermore, the effects of Prdx2 resulted in an altered expression of stemness associated with the Hh/Gli1 signaling pathway. Finally, knockdown of Prdx2 in CD133+ cells reduced the volume of xenograft tumors in BALB/c-nu mice. Taken together, colon CSCs overexpress Prdx2, which promotes their stem cell properties via the Hh/Gli1 signaling pathway. The results suggest that Prdx2 may be an effective therapeutic target for the elimination of CSCs in colorectal cancer.
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