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WNT10A 耗竭通过抑制微血管和胶原表达来预防肿瘤生长。

Depletion of WNT10A Prevents Tumor Growth by Suppressing Microvessels and Collagen Expression.

机构信息

Department of Pathology and Laboratory Medicine, Kanazawa Medical University, Ishikawa 920-0293, Japan.

Shared-Use Research Center, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.

出版信息

Int J Med Sci. 2019 Jan 29;16(3):416-423. doi: 10.7150/ijms.26997. eCollection 2019.

Abstract

: 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 regulatory functions of WNT10A in tumor growth, we examined the net effects of WNT10A depletion using -deficient mice ( ). : We subjected C57BL/6J wild-type (WT) or mice to murine melanoma B16-F10 cell transplantation. mice showed a significantly smaller volume of transplanted melanoma as well as fewer microvessels and less collagen expression and more necrosis than WT mice. : Taken together, our observations suggest that critical roles of -depleted anti-stromagenesis prevent tumor growth, in contrast with true wound healing/scarring.

摘要

我们最近报道称,WNT10A 通过调节胶原蛋白的表达/合成在伤口愈合中起着关键作用,因为 WNT10A 的耗竭会显著延迟皮肤溃疡的形成。WNT 信号也与癌症微环境和增殖密切相关,因为肿瘤实际上被认为是“未愈合”或“过度愈合”的伤口。为了确定 WNT10A 在肿瘤生长中的调节功能,我们使用 缺陷小鼠()检查了 WNT10A 耗竭的净效应。我们使 C57BL/6J 野生型(WT)或 缺陷小鼠接受黑色素瘤 B16-F10 细胞移植。与 WT 小鼠相比,缺陷小鼠移植的黑色素瘤体积明显较小,微血管较少,胶原蛋白表达较少,坏死较多。综上所述,我们的观察结果表明,-耗竭的抗基质作用阻止了肿瘤生长,与真正的伤口愈合/瘢痕形成形成对比。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a674/6428976/2a22beb8fbec/ijmsv16p0416g001.jpg

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