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QKI, a miR-200 target gene, suppresses epithelial-to-mesenchymal transition and tumor growth.

Int. J. Cancer. 2019 Sep 15;145(6):1585-1595. doi:10.1002/ijc.32372. Epub 2019 May 14
Eun Ju Kim 1 , Jeong Seon Kim 1 , Sieun Lee 1 , Heejin Lee 2 , Jung-Sook Yoon 3 , Ji Hyung Hong 4 , Sang Hoon Chun 4 , Der Sheng Sun 4 , Hye Sung Won 4 , Soon Auck Hong 5 , Keunsoo Kang 6 , Jeong Yeon Jo 7 , Minyoung Choi 7 , Dong Hoon Shin 7 , Young-Ho Ahn 1 , Yoon Ho Ko 4
Eun Ju Kim 1 , Jeong Seon Kim 1 , Sieun Lee 1 , Heejin Lee 2 , Jung-Sook Yoon 3 , Ji Hyung Hong 4 , Sang Hoon Chun 4 , Der Sheng Sun 4 , Hye Sung Won 4 , Soon Auck Hong 5 , Keunsoo Kang 6 , Jeong Yeon Jo 7 , Minyoung Choi 7 , Dong Hoon Shin 7 , Young-Ho Ahn 1 , Yoon Ho Ko 4
+ et al

[No authors listed]

Author information
  • 1 Department of Molecular Medicine and Tissue Injury Defense Research Center, College of Medicine, Ewha Womans University, Seoul, South Korea.
  • 2 Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
  • 3 Clinical Research Laboratory, Uijeongbu St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Uijeongbu, Gyeonggi, South Korea.
  • 4 Division of Oncology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, South Korea.
  • 5 Department of Pathology, College of Medicine, Chung-Ang University, Seoul, South Korea.
  • 6 Department of Microbiology, College of Natural Sciences, Dankook University, Cheonan, Chungnam, South Korea.
  • 7 Research Institute and Department of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang, Gyeonggi, South Korea.

摘要


The microRNA-200 (miR-200) family plays a major role in specifying epithelial phenotype by preventing expression of the transcription repressors ZEB1 and ZEB2, which are well-known regulators of the epithelial-to-mesenchymal transition (EMT) in epithelial tumors including oral squamous cell carcinoma (OSCC). Here, we elucidated whether miR-200 family members control RNA-binding protein quaking (QKI), a newly identified tumor suppressor that is regulated during EMT. We predicted that miR-200a and miR-200b could recognize QKI 3'-UTR by analyzing TargetScan and The Cancer Genome Atlas head and neck squamous cell carcinoma (HNSCC) dataset. Forced expression of miR-200b/a/429 inhibited expression of ZEB1/2 and decreased cell migration in OSCC cell lines CAL27 and HSC3. QKI expression was also suppressed by miR-200 overexpression, and the 3'-UTR of QKI mRNA was directly targeted by miR-200 in luciferase reporter assays. Interestingly, shRNA-mediated knockdown of QKI led to pronounced EMT and protumor effects in both in vitro and in vivo studies of OSCC. Furthermore, high expression of QKI protein is associated with favorable prognosis in surgically resected HNSCC and lung adenocarcinoma. In conclusion, QKI increases during EMT and is targeted by miR-200; while, it suppresses EMT and tumorigenesis. We suggest that QKI and miR-200 form a negative feedback loop to maintain homeostatic responses to EMT-inducing signals.

KEYWORDS: QKI, epithelial-to-mesenchymal transition, lung cancer, miRNA-200, oral cancer