4.7 Article

Downregulation of Wnt3 Suppresses Colorectal Cancer Development Through Inhibiting Cell Proliferation and Migration

期刊

FRONTIERS IN PHARMACOLOGY
卷 10, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2019.01110

关键词

Wnt3; colorectal cancer; HCT-116; proliferation; apoptosis; glycolysis

资金

  1. National Natural Science Foundation of China [81472232, 81970726, 81270522, 81700731, 81672433, 81970551, 81370537]
  2. Program for Science & Technology Innovation Talents in Universities of Henan Province (HASTIT) [13HASTIT024]
  3. Plan for Scientific Innovation Talent of Henan Province
  4. Henan Provincial Natural Science Foundation [162300410034]
  5. Scientific Research Fund of Henan University [2015YBZR051]
  6. Fundamental Research Funds for the Central Universities [PYBZ1706, XK1802-8, PYBZ1803]
  7. Research Projects on Biomedical Transformation of China-Japan Friendship Hospital [PYBZ1803]

向作者/读者索取更多资源

The aberrant expression of Wnt3 has linked to several types of human malignancies. However, it is not known for its role in tumorigenesis of colorectal cancer (CRC). Herein, we show that Wnt3 is upregulated in human CRC tissues and is essential for the CRC progression. Knockdown of Wnt3 in human CRC cells delayed tumor formation in nude mouse xenografts through silencing of canonical Wnt pathway and glycolysis. We further found that silencing of Wnt3 enhanced the sensitivity of CRC cells to cisplatin through inducing apoptotic cell death. Taken together, it demonstrates that Wnt3 is a novel clinical biomarker for the detection of CRC and plays an important role in colorectal tumorigenesis. Therefore, downregulation of Wnt3 will be a valuable strategy in CRC treatment.

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