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II型跨膜丝氨酸蛋白酶4（TMPRSS4）通过激活丝裂原活化蛋白激酶（MAPK）和蛋白激酶B（AKT）促进子宫内膜癌细胞（HEC1A和Ishikawa）的增殖、侵袭和上皮-间质转化。

Type II transmembrane serine proteases 4 (TMPRSS4) promotes proliferation, invasion and epithelial-mesenchymal transition in endometrial carcinoma cells (HEC1A and Ishikawa) via activation of MAPK and AKT.

作者信息

Xiao Huan, Zhang Zhian, Peng Dan, Wei Chunqing, Ma Benling

机构信息

Department of Gynaecology and Obstetrics, Huanggang Central Hospital Affiliated to Changjiang University, Huanggang, People's Republic of China.

Department of Gynaecology and Obstetrics, The Second Affiliated Hospital of Hunan University of Chinese Medicine, Changsha, People's Republic of China.

出版信息

Anim Cells Syst (Seoul). 2021 Jun 25;25(4):211-218. doi: 10.1080/19768354.2021.1944311. eCollection 2021.

DOI:10.1080/19768354.2021.1944311
PMID:34408809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8366621/
Abstract

Endometrial cancer is the most common gynecological cancer in the developed countries. Type II transmembrane serine proteases 4 (TMPRSS4) is a newly discovered transmembrane protein, which may be related to the invasion, metastasis of the tumor and the poor prognosis. This study aims to investigate the role of TMPRSS4 in endometrial cancer and the detailed molecular mechanism. The results showed that TMPRSS4 was highly expressed in human endometrial cancer cells (HEC1A and Ishikawa). TMPRSS4 knockdown inhibited proliferation of endometrial cancer cells. In TMPRSS4 knockdown cells, the invasion of cells was significantly supressed. The expression of E-cadherin was significantly enhanced, while the levels of fibronectin and vimentin decreased in TMPRSS4 knockdown cells, which indicated thatTMPRSS4 knockdown attenuated the EMT of cancer cells. TMPRSS4 positively regulated the activation of MAPK and AKT signaling pathways in endometrial cancer. In conclusion, this study indicated that TMPRSS4 may be associated with the progression of endometrial cancer through promoting proliferation, invasion and EMT via activation of MAPK and AKT in endometrial cancer cells. TMPRSS4 may be a new and more effective target or therapeutic strategy for treating endometrial cancer.

摘要

子宫内膜癌是发达国家最常见的妇科癌症。II型跨膜丝氨酸蛋白酶4（TMPRSS4）是一种新发现的跨膜蛋白，可能与肿瘤的侵袭、转移及预后不良有关。本研究旨在探讨TMPRSS4在子宫内膜癌中的作用及详细分子机制。结果显示，TMPRSS4在人子宫内膜癌细胞（HEC1A和Ishikawa）中高表达。敲低TMPRSS4可抑制子宫内膜癌细胞增殖。在敲低TMPRSS4的细胞中，细胞侵袭明显受到抑制。E-钙黏蛋白表达显著增强，而纤连蛋白和波形蛋白水平在敲低TMPRSS4的细胞中降低，这表明敲低TMPRSS4可减弱癌细胞的上皮-间质转化（EMT）。TMPRSS4正向调节子宫内膜癌中MAPK和AKT信号通路的激活。总之，本研究表明TMPRSS4可能通过激活子宫内膜癌细胞中的MAPK和AKT促进增殖、侵袭和EMT，从而与子宫内膜癌的进展相关。TMPRSS4可能是治疗子宫内膜癌的一种新的、更有效的靶点或治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/b4d5ec238a6a/TACS_A_1944311_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/65caa6d12a41/TACS_A_1944311_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/bf5c2c7b0b10/TACS_A_1944311_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/b566bab33073/TACS_A_1944311_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/b4d5ec238a6a/TACS_A_1944311_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/65caa6d12a41/TACS_A_1944311_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/bf5c2c7b0b10/TACS_A_1944311_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/b566bab33073/TACS_A_1944311_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7375/8366621/b4d5ec238a6a/TACS_A_1944311_F0004_OC.jpg

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