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Supplementary Figures S1-S9 from Cytosolic TMEM88 Promotes Invasion and Metastasis in Lung Cancer Cells by Binding DVLS

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posted on 2023-03-30, 23:04 authored by Xiupeng Zhang, Xinmiao Yu, Guiyang Jiang, Yuan Miao, Liang Wang, Yong Zhang, Yang Liu, Chuifeng Fan, Xuyong Lin, Qianze Dong, Qiang Han, Huanyu Zhao, Yong Han, Xu Han, Xuezhu Rong, Shuting Ding, Endi Wang, Enhua Wang
<p>Supplementary Figures S1-S9: Supplementary FigureS1: Expression and localization of TMEM88 in epithelial malignancies and non-small cell lung cancer (NSCLC) cell lines Supplementary FigureS2: Effect of TMEM88 on canonical Wnt signaling and expression of its downstream target genes Supplementary FigureS3: Co-localization of and interaction between TMEM88 and DVLS in different cellular compartments Supplementary FigureS4: Effects of TMEM88 on proliferation, migration, and invasion of NSCLC cells with cytosolic TMEM88 Supplementary FigureS5: Effects of TMEM88 on proliferation and invasion of non-small cell lung cancer cells Supplementary FigureS6: Effects of cytosolic TMEM88 on expression of epithelial-mesenchymal transition (EMT) proteins Supplementary FigureS7: Effect of TMEM88 and DVLS co-transfection on expression of Snail and invasion in NSCLC cells Supplementary FigureS8: Effects of co-transfecting TMEM88 and DVLS on proteins involved in Snail stabilization Supplementary FigureS9: Overexpression of TMEM88 did not influence expression of Snail, occludin, or ZO-1 in cells with membrane-bound TMEM88</p>

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ARTICLE ABSTRACT

Transmembrane protein 88 (TMEM88) is a transmembrane protein that plays a crucial role in regulating human stem cell differentiation and embryonic development. However, its expression and clinicopathologic significance in human neoplasms is unclear. In this study, the expression and subcellular localizations of TMEM88 were assessed in 214 cases of non–small cell lung cancer (NSCLC). Notably, TMEM88 was highly expressed in the cytosol of ∼60% NSCLC specimens examined. Higher expression of cytosolic TMEM88 in NSCLC correlated significantly with poor differentiation, high TNM stage, lymph node metastasis, and inferior survival. In NSCLC cells displaying membrane-localized TMEM88, we observed an inhibition of canonical Wnt signaling due to interactions of TMEM88 with the Wnt pathway factor Dishevelled (DVLS). In contrast, NSCLC cells with cytosol-localized TMEM88 lacked effects on Wnt signaling. Cytosolic interactions of TMEM88 and DVLS increased the expression of phosphorylated, active forms of p38, GSK3β (Thr390), and Snail, thereby reducing the expression of the tight junction-associated proteins ZO-1 and occludin, effects associated with enhanced invasive and metastatic cell characters. Importantly, attenuating the expression of cytosolic TMEM88 reduced metastatic prowess in xenograft models. Overall, our findings show how mislocalization of TMEM88 to the cytosol in NSCLC cells ablates its Wnt pathway regulatory properties, thereby promoting invasion and metastasis by activating the p38–GSK3β–Snail signaling pathway. Cancer Res; 75(21); 4527–37. ©2015 AACR.

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    Lung CancerProgression, Invasion & MetastasisMetastasis

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