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. 2025 Jul 11;15(16):7940–7955. doi: 10.7150/thno.109442

Figure 2.

Figure 2

Activation of the UPR drives EMT in human lens epithelial cells. (A) Western blotting and quantification of the UPR markers BIP, CHOP, ATF6, and c-ATF6; the EMT markers FN, N-cadherin, and SNAI1; and the epithelial cell marker E-cadherin (n = 5). The asterisk denotes an unglycosylated form of full-length ATF6 due to TM treatment. Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001. (B) qPCR and quantification of HSPA5, ATF6, FN, and SNAI1 expression (n = 5). Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001. (C) Immunofluorescence staining of ATF6 and SNAI1. Scale bars, 50 μm. (D) Nuclear protein fraction analysis (n = 5). Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001. (E) Migration of HLE-B3 cells stimulated with TM was assessed using wound healing and transwell assays. Scale bars, 50 μm. (F) Quantification of wound closure and the number of migrating cells (n = 5). Data are presented as mean ± SEM; *p < 0.05, **p < 0.01, ***p < 0.001.