Research Papers:

Peroxiredoxin 2 is essential for maintaining cancer stem cell-like phenotype through activation of Hedgehog signaling pathway in colon cancer

Rong Wang _, Jinlai Wei, Shouru Zhang, Xingye Wu, Jinbao Guo, Maoxi Liu, Kunli Du, Jun Xu, Linglong Pen, Zhenbing Lv, Wenxian You, Yongfu Xiong and Zhongxue Fu

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Oncotarget. 2016; 7:86816-86828. https://doi.org/10.18632/oncotarget.13559

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Rong Wang1, Jinlai Wei1, Shouru Zhang1, Xingye Wu1, Jinbao Guo1, Maoxi Liu1, Kunli Du1, Jun Xu1, Linglong Peng1, Zhenbing Lv1, Wenxian You1, Yongfu Xiong1, Zhongxue Fu1

1Department of Gastrointestinal Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China

Correspondence to:

Zhongxue Fu, email: [email protected]

Keywords: Prdx2, stemness, cancer stem cell, Hedgehog, colon cancer

Received: August 10, 2016     Accepted: November 11, 2016     Published: November 24, 2016


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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