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This study highlights that TMEPAI decreases c-Maf stability by recruiting the ubiquitin ligase NEDD4 to c-Maf for proteasomal degradation in myeloma cells.
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JHY-A007-50 mediates the downregulation of TMEPAI expression.
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describe recent progresses in the understanding of how the TMEPAI family physiologically contributes to cellular functions and diseases
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binding of SMAD2/3, the intracellular effectors of activin signaling, was significantly enriched at the Pmepa1 gene, which encodes a negative feedback regulator of TGF-beta signaling in cancer cells, and at the Kdm6b gene, which encodes an epigenetic regulator promoting transcriptional plasticity.
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study showed that the inhibition of autophagy induced by the depletion of TMEPAI is involved in regulation of Beclin-1.
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these findings indicated that PMEPA1 participates in TGF-beta- and hypoxia-regulated gene expression networks in solid tumors and thereby may contribute to tumor progression.
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the present study suggest that the upregulation of miR19a3p expression levels contributes to tumor progression and that one of its underlying mechanisms involves inhibition of PMEPA1 expression.
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Sp1 up-regulated TMEPAI protein expression, as well as Sp1 promoting TMEPAI-induced cell proliferation.
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PMEPA1 was upregulated in breast cancer cell lines as well as in a set of clinical invasive breast ductal carcinomas. Interestingly, depletion of PMEPA1 decreased breast cancer stem cell (CSC)-enriched populations, while ectopic overexpression of PMEPA1 increased breast CSC-enriched populations.
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these data elaborated on the diverse activity among TCF/LEF family members with respect to the transcriptional regulation of the TMEPAI gene.
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Data show that over-expressed transmembrane prostate androgen-induced protein 1 (PMEPA1) can promote cell migration and maintain the mesenchymal-like morphology of breast cancer cells.
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Data show that silencing of PMEPA1 protein facilitates the growth of prostate cancer cells and modulates androgen receptor (AR) through NEDD4 ubiquitin protein ligase and PTEN protein.
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Downregulation of PMEPA1 may result in increased androgen receptor protein levels and function in cancer of the prostate cells, contributing to prostate tumorigenesis.
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EGF signaling collaboratively regulates TGF-beta-induced TMEPAI expression.
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TMEPAI is translocated on the lysosome and late endosome, and that association with Nedd4 is required for the transport of TMEPAI to the lysosome.
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TMEPAI promotes tumorigenic activities in lung cancer cells.
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The levels of TMEPAI in lung tumor tissues are very high.
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Differentially expressed genes were identified, including E-cadherin, IL-8 and STAG1/PMEPA1 in an androgen-independent prostate cancer PC3 subclone.
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Results suggest that TMEPAI functions in breast cancer as a molecular switch that converts TGF-beta from a tumor suppressor to a tumor promoter.
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Expression of PMEPA1 was well maintained both in colon cancer primary tumors and in colon cancer liver metastases.
