Nuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea

Ma, Wenbei; Xie, Zhengyuan; Chen, Hui; Zeng, Lirong; Chen, Xiaohong; Feng, Songfu; Lu, Xiaoyan

doi:10.1177/1535370220983243

Cited by 6 publications

(3 citation statements)

References 40 publications

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“…Consequently, our observations implied that the MICAL2mediated downregulation of E-cadherin protein levels may be the primary inducer of β-catenin nuclear translocation. This decrease in E-cadherin content was consistent with the results of Ma et al [32], who showed that high glucose levels induced the degradation of E-cadherin in corneal epithelial cells, subsequently leading to reduced β-catenin/E-cadherin complex formation and the promotion of β-catenin nuclear translocation. That Fig.…”

Section: Discussionsupporting

confidence: 92%

MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway

Wang

Min

et al. 2022

Cell Commun Signal

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Background Gastric cancer is a common and lethal human malignancy worldwide and cancer cell metastasis is the leading cause of cancer-related mortality. MICAL2, a flavoprotein monooxygenase, is an important regulator of epithelial-to-mesenchymal transition. The aim of this study was to explore the effects of MICAL2 on gastric cancer cell migration and determine the underlying molecular mechanisms. Methods Cell migration was examined by wound healing and transwell assays. Changes in E-cadherin/β-catenin signaling were determined by qPCR and analysis of cytoplasmic and nuclear protein fractions. E-cadherin/β-catenin binding was determined by co-immunoprecipitation assays. Cdc42 activity was examined by pulldown assay. Results MICAL2 was highly expressed in gastric cancer tissues. The knockdown of MICAL2 significantly attenuated migratory ability and β-catenin nuclear translocation in gastric cancer cells while LiCl treatment, an inhibitor of GSK3β, reversed these MICAL2 knockdown-induced effects. Meanwhile, E-cadherin expression was markedly enhanced in MICAL2-depleted cells. MICAL2 knockdown led to a significant attenuation of E-cadherin ubiquitination and degradation in a Cdc42-dependent manner, then enhanced E-cadherin/β-catenin binding, and reduced β-catenin nuclear translocation. Conclusions Together, our results indicated that MICAL2 promotes E-cadherin ubiquitination and degradation, leading to enhanced β-catenin signaling via the disruption of the E-cadherin/β-catenin complex and, consequently, the promotion of gastric cell migration.

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Section: Discussionsupporting

confidence: 92%

MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway

Wang

Min

et al. 2022

Cell Commun Signal

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“…The maintenance of appropriate cell adhesion is crucial for cell migration and wound healing. A previous study reported that the E-cadherin/β-catenin complex is involved in the adhesion of corneal epithelial cells and high glucose induced decreased expression of E-cadherin and β-catenin in mouse corneal epithelial cells, as well as reducing the formation of β-catenin/E-cadherin complex ( 20 ). β-catenin plays an essential role in the Wnt/β-catenin pathway.…”

Section: Discussionmentioning

confidence: 99%

Lithium chloride promotes diabetic corneal epithelial wound healing by activating the Wnt/β‑catenin signaling pathway

Jing

Tan²,

et al. 2023

Exp Ther Med

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Corneal epithelial abnormality is a common manifestation of diabetic keratopathy and leads to delayed epithelial wound healing. The Wnt/β-catenin signaling pathway participates in the development, differentiation and stratification of corneal epithelial cells. The present study compared the expression of Wnt/β-catenin signaling pathway related factors, including Wnt7a, β-catenin, cyclin D1 and phosphorylated (p-) glycogen synthase kinase 3 β (Gsk3b) between normal and diabetic mouse corneas, by reverse transcription-quantitative PCR, western blotting and immunofluorescence staining. It was found that the expression of the Wnt/β-catenin signaling pathway related factors was downregulated in diabetic corneas. Upon corneal epithelium scraping, the wound healing rate was significantly increased in diabetic mice after topical treatment with lithium chloride. After further investigation, significantly upregulated levels of Wnt7a, β-catenin, cyclin D1 and p-Gsk3b were found in the diabetic group 24 h after treatment, accompanied by β-catenin nuclear translocation observed by immunofluorescence staining. These results suggest that active Wnt/β-catenin pathway can promote diabetic corneal epithelial wound healing.

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“…Studies of recurrent erosions in animal models have allowed us to gain insight into how erosions form and to develop improved treatments [6][7][8][9][10][11]. While the mouse cornea lacks a thick Bowman's layer under its epithelial basement membrane (EBM), studies using the mouse cornea have, nevertheless, shown how important the interaction between corneal epithelial cells and the basement membrane is in re-establishing homeostasis after corneal injury [6,7].…”

Section: Introductionmentioning

confidence: 99%

Immune Cells Localize to Sites of Corneal Erosions in C57BL/6 Mice

Pal‐Ghosh

Menko

et al. 2023

Biomolecules

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Recurrent epithelial erosions develop in the cornea due to prior injury or genetic predisposition. Studies of recurrent erosions in animal models allow us to gain insight into how erosions form and are resolved. While slowing corneal epithelial cell migration and reducing their proliferation following treatment with mitomycin C reduce erosion formation in mice after sterile debridement injury, additional factors have been identified related to cytokine expression and immune cell activation. The relationship between recruitment of immune cells to the region of the cornea where erosions form and their potential roles in erosion formation and/or erosion repair remains unexplored in the C57BL/6 mouse recurrent erosion model. Here, high resolution imaging of mouse corneas was performed at D1, D7, and D28 after dulled-blade debridement injury in C57BL/6 mice. Around 50% of these mice have frank corneal erosions at D28 after wounding. A detailed assessment of corneas revealed the involvement of M2 macrophages in both frank and developing erosions at early stages of their formation.

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Nuclear translocation of β-catenin induced by E-cadherin endocytosis causes recurrent erosion of diabetic cornea

Cited by 6 publications

References 40 publications

MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway

MICAL2 contributes to gastric cancer cell migration via Cdc42-dependent activation of E-cadherin/β-catenin signaling pathway

Lithium chloride promotes diabetic corneal epithelial wound healing by activating the Wnt/β‑catenin signaling pathway

Immune Cells Localize to Sites of Corneal Erosions in C57BL/6 Mice

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