Knockdown of ER‐α36 expression inhibits glioma proliferation, invasion and epithelial‐to‐mesenchymal transition. Issue 2 (11th August 2021)

• Record Type: Journal Article
• Authors: Zhao, Bowen; Ye, Xiang; Yang, Yuanyuan; Wang, Yuxing; Wang, Ru; Pan, Xiaohua; Wang, Molin
• Is Part Of: Anatomical record. Volume 305:Issue 2(2022)
• Page Start: 321
• Page End: 332
• Publication Date: 2021-08-11
• Subjects: ER‐α36 -- glioma -- invasion -- proliferation; Anatomy -- Periodicals; Evolution (Biology) -- Periodicals; Morphology -- Periodicals; 571.3
• DOI: 10.1002/ar.24723
• Languages: English
• ISSNs: 1932-8486

Abstract

Abstract: Estrogen receptor‐α36 (ER‐α36), a subtype of the estrogen receptor, is reported to play roles in tumorigenesis and tamoxifen resistance in several tumors, especially breast cancer. However, the role of ER‐α36 in glioma proliferation and invasion remains unknown. Here, we explored the function of ER‐α36 in glioma cells, using U87 and U251 cell lines. We found that ER‐α36 was upregulated in glioma tissues compared to adjacent nontumor tissues. In U87 and U251 glioma cell lines, inhibition of ER‐α36 expression by shRNA suppressed cell proliferation and invasion. In addition, the expression of an epithelial marker, ZO‐1, was upregulated while that of one mesenchymal marker, N‐cadherin, was downregulated with ER‐α36 knockdown. We also found that inhibition of ER‐α36 inactivated both PI3K/AKT and MEK/ERK signals. Taken together, these data indicated that overexpression of ER‐α36 is associated with glioma proliferation and progression but that inhibition of ER‐α36 leads to suppressed invasion and the epithelial‐to‐mesenchymal transition via PI3K/AKT and MEK/ERK pathway inactivation in glioma cells.