Int J Med Sci 2019; 16(3):416-423. doi:10.7150/ijms.26997 This issue Cite
Research Paper
1. Department of Pathology and Laboratory Medicine, Kanazawa Medical University, Ishikawa 920-0293, Japan
2. Shared-Use Research Center, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan
3. Department of Occupational Pneumology, School of Medicine, University of Occupational and Environmental Health
4. Department of Orthopaedic Surgery, School of Medicine, University of Occupational and Environmental Health
5. Department of Human, Information and Life Sciences, School of Medicine, University of Occupational and Environmental Health
6. Department of Thoracic Surgery, Kanazawa Medical University, Ishikawa 920-0293, Japan
7. Department of Pathology and Cell Biology, School of Medicine, University of Occupational and Environmental Health
8. Laboratory of Pathology, Fukuoka Tokushukai Hospital, Fukuoka 816-0864, Japan
9. Asahi-Matsumoto Hospital, Kitakyushu 800-0242, Japan.
Background: We recently reported that WNT10A plays a pivotal role in wound healing by regulating collagen expression/synthesis, as the depletion of WNT10A dramatically delays skin ulcer formation. WNT signaling also has a close correlation with the cancer microenvironment and proliferation, since tumors are actually considered to be 'unhealing' or 'overhealing' wounds. To ascertain the in vivo regulatory functions of WNT10A in tumor growth, we examined the net effects of WNT10A depletion using Wnt10a-deficient mice (Wnt10a-/-).
Methods and Results: We subjected C57BL/6J wild-type (WT) or Wnt10a-/- mice to murine melanoma B16-F10 cell transplantation. Wnt10a-/- mice showed a significantly smaller volume of transplanted melanoma as well as fewer microvessels and less collagen expression and more necrosis than WT mice.
Conclusions: Taken together, our observations suggest that critical in vivo roles of Wnt10a-depleted anti-stromagenesis prevent tumor growth, in contrast with true wound healing/scarring.
Keywords: WNT10A, Wnt10a-deficient mice (Wnt10a-/-), tumor growth, microvessel, collagen expression