子宫内膜异位症患者中S100A6的上调及其在异位子宫内膜间质细胞中的作用。
Upregulation of S100A6 in patients with endometriosis and its role in ectopic endometrial stromal cells.
作者信息
Peng Yaoming, Lin Jiabin, Ma Junyan, Lin Kaiqing, Xu Kaihong, Lin Jun
机构信息
a Department of Gynecology and Obstetrics , Women's Hospital, Zhejiang University Medical College , Hangzhou , P.R. China.
b Department of Laboratory , Women's Hospital, School of Medicine, Zhejiang University , Hangzhou , P.R. China.
出版信息
Gynecol Endocrinol. 2018 Sep;34(9):815-820. doi: 10.1080/09513590.2018.1451506. Epub 2018 Mar 16.
S100 calcium-binding protein A6 (S100A6) is up-regulated in many malignancies and overexpression of S100A6 has been identified associated with proliferation, migration and invasion phenotype in several cancer cells. In the present study, we explored whether S100A6 plays a role in the development of endometriosis. Significantly higher levels of mRNA and protein expression of S100A6 were observed in ectopic endometrial tissues compared to eutopic and normal endometrial tissues. Silencing of S100A6 in ectopic endometrial stromal cells (ESCs) significantly inhibited cell viability, migration and invasion. Moreover, knockdown of S100A6 suppressed p38/MAPK activity in ectopic ESCs, which can be partially attenuated by CacyBP/SIP phosphorylation inhibitor. In conclusion, our results suggest that the abnormal expression of S100A6 may contribute to the pathogenesis of endometriosis and the S100A6/CacyBP/p38 signaling may provide as a promising treatment target.
S100钙结合蛋白A6（S100A6）在许多恶性肿瘤中上调，并且已确定S100A6的过表达与几种癌细胞的增殖、迁移和侵袭表型相关。在本研究中，我们探讨了S100A6是否在子宫内膜异位症的发生发展中起作用。与在位和正常子宫内膜组织相比，在异位子宫内膜组织中观察到S100A6的mRNA和蛋白表达水平显著更高。异位子宫内膜基质细胞（ESC）中S100A6的沉默显著抑制了细胞活力、迁移和侵袭。此外，S100A6的敲低抑制了异位ESC中的p38/丝裂原活化蛋白激酶（MAPK）活性，而这种抑制可被CacyBP/SIP磷酸化抑制剂部分减弱。总之，我们的结果表明，S100A6的异常表达可能有助于子宫内膜异位症的发病机制，并且S100A6/CacyBP/p38信号通路可能成为一个有前景的治疗靶点。
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