Promotion of the occurrence of endometrioid carcinoma by S100 calcium binding protein P.
Promotion of the occurrence of endometrioid carcinoma by S100 calcium binding protein P.
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S100钙结合蛋白P促进子宫内膜样癌的发生
DOI：
10.1186/s12885-020-07350-x
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发表时间：
2020-09-03
期刊：
影响因子：
3.8
通讯作者：
Zhang W
中科院分区：
文献类型：
--
作者：
Zhang D;Chen X;Xia H;Wang L;Zhao H;Xu B;Zhang A;Zhang W
子宫内膜癌是最常见的恶性肿瘤，是对子宫内膜癌的严重威胁目前的研究旨在研究子宫内膜癌及其前体病变中S100P的表达，并探索可能的机制。
我们还收集了正常子宫内膜的石蜡，简单和复杂的非型增生，非典型增生和子宫内膜类药物癌。线（Ishikawa和RL95–2），并观察到S100p在这些细胞中的表达。观察S100P的共定位及其相互作用的蛋白EZRIN在RL95-2细胞中使用。
随着疾病从正常子宫内膜和简单的非型增生，S100p信号的级增加，到复杂的非型增生，非典型增生，然后在子宫内膜癌中分布。在子宫内膜癌细胞中脱落S100p，F-肌动蛋白在细胞核中或局部细胞膜中均匀Ishikawa细胞中的S100p降低了其细胞侵袭能力，而子宫内膜基质细胞中的S100P过表达增加了细胞的侵袭。
这些数据表明，通过与Ezrin的相互作用和F-肌动蛋白的重组以促进细胞浸润，S100P可能参与子宫内膜癌的发生和发展。
Endometrial cancer, one of the most common malignant tumors, is a serious threat to women’s health. Endometrial hyperplasia is a precursor of endometrial cancer. S100 calcium binding protein P (S100P) has been found to play important roles in many types of cancer. The present study aimed to investigate the expression of S100P in endometrial cancer and its precursor lesions, and to explore the possible mechanisms. We collected paraffin sections of normal endometrium, simple and complex non-atypical hyperplasia, atypical hyperplasia, and endometrioid carcinoma. The expression of S100P in endometrial cancer and its precancerous lesions was observed using immunohistochemistry. We also cultured primary endometrial cells and endometrial cancer cell lines (Ishikawa and RL95–2), and observed the expression of S100P in these cells. Laser confocal microscopy was used to observe the co-localization of S100P and its interacting protein Ezrin in RL95–2 cells. We employed lentiviruses to knockdown and overexpress S100P and then detected the F-actin distribution and cell invasion using phalloidin staining and Transwell assays. There was a gradual increase in the S100P signal as the disease progressed from normal endometrium and simple non-atypical hyperplasia, to complex non-atypical hyperplasia, atypical hyperplasia, and then to endometrial cancer. S100P was mainly distributed in the cytoplasm and co-localized with Ezrin in endometrial cancer cells. After knocking down S100P, F-actin aggregated in the nucleus or to the local cell membrane. Furthermore, knockdown of S100P in Ishikawa cells decreased their cell invasion capability. Meanwhile, S100P overexpression in endometrial stromal cells increased cell invasion. These data suggested that S100P might be involved in the occurrence and development of endometrial cancer via interaction with Ezrin and re-organization of F-actin to promote cell invasion.
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影响因子：
3.3
作者：
Koltzscher, M;Neumann, C;Gerke, V
通讯作者：
Gerke, V
S100P 增强人滋养层细胞系的运动性和侵袭性。
影响因子：
4.6
作者：
Tabrizi MEA;Lancaster TL;Ismail TM;Georgiadou A;Ganguly A;Mistry JJ;Wang K;Rudland PS;Ahmad S;Gross SR
通讯作者：
Gross SR
影响因子：
11.2
作者：
Whiteman, Hannah J.;Weeks, Mark E.;Crnogorac-Jurcevic, Tatjana
通讯作者：
Crnogorac-Jurcevic, Tatjana
DOI：
10.1186/1477-7827-10-106
发表时间：
2012-12-07
期刊：
Reproductive biology and endocrinology : RB&E
影响因子：
--
作者：
Zhang D;Ma C;Sun X;Xia H;Zhang W
通讯作者：
Zhang W
影响因子：
4.6
作者：
Wang Z;Risch H;Lu L;Irwin ML;Mayne S;Schwartz P;Rutherford T;De Vivo I;Yu H
通讯作者：
Yu H