Journal
FRONTIERS IN PHARMACOLOGY
Volume 10, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2019.01110
Keywords
Wnt3; colorectal cancer; HCT-116; proliferation; apoptosis; glycolysis
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Funding
- National Natural Science Foundation of China [81472232, 81970726, 81270522, 81700731, 81672433, 81970551, 81370537]
- Program for Science & Technology Innovation Talents in Universities of Henan Province (HASTIT) [13HASTIT024]
- Plan for Scientific Innovation Talent of Henan Province
- Henan Provincial Natural Science Foundation [162300410034]
- Scientific Research Fund of Henan University [2015YBZR051]
- Fundamental Research Funds for the Central Universities [PYBZ1706, XK1802-8, PYBZ1803]
- Research Projects on Biomedical Transformation of China-Japan Friendship Hospital [PYBZ1803]
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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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