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- W4362542034 abstract "<div>Abstract<p>Progression of benign tumors to invasive, metastatic cancer is accompanied by the epithelial-to-mesenchymal transition (EMT), characterized by loss of the cell-adhesion protein E-cadherin. Although silencing mutations and transcriptional repression of the E-cadherin gene have been widely studied, not much is known about posttranslational regulation of E-cadherin in tumors. We show that E-cadherin is tightly coexpressed with the secretory pathway Ca<sup>2+</sup>-ATPase isoform 2, SPCA2 (<i>ATP2C2</i>), in breast tumors. Loss of SPCA2 impairs surface expression of E-cadherin and elicits mesenchymal gene expression through disruption of cell adhesion in tumorspheres and downstream Hippo-YAP signaling. Conversely, ectopic expression of SPCA2 in triple-negative breast cancer elevates baseline Ca<sup>2+</sup> and YAP phosphorylation, enhances posttranslational expression of E-cadherin, and suppresses mesenchymal gene expression. Thus, loss of SPCA2 phenocopies loss of E-cadherin in the Hippo signaling pathway and EMT–MET transitions, consistent with a functional role for SPCA2 in E-cadherin biogenesis. Furthermore, we show that SPCA2 suppresses invasive phenotypes, including cell migration <i>in vitro</i> and tumor metastasis <i>in vivo</i>. Based on these findings, we propose that SPCA2 functions as a key regulator of EMT and may be a potential therapeutic target for treatment of metastatic cancer.</p>Implications:<p>Posttranslational control of E-cadherin and the Hippo pathway by calcium signaling regulates EMT in breast cancer cells.</p></div>" @default.
- W4362542034 created "2023-04-06" @default.
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- W4362542034 date "2023-04-03" @default.
- W4362542034 modified "2023-09-29" @default.
- W4362542034 title "Data from A Ca<sup>2+</sup>-ATPase Regulates E-cadherin Biogenesis and Epithelial–Mesenchymal Transition in Breast Cancer Cells" @default.
- W4362542034 doi "https://doi.org/10.1158/1541-7786.c.6541257" @default.
- W4362542034 hasPublicationYear "2023" @default.
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