IndraLab

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PSMD14 activates TGFB. 7 / 7
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"Concurrently, gene set enrichment analyses of the TCGA and several GEO liver cancer datasets demonstrated a significant enrichment in the expression of a set of genes, which indicates poor survival of patients [32], in HCCs with high POH1 expression (Fig. S2b).3.2 POH1 promotes TGF-beta signaling in HCC cells."

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"POH1 can remove the K63-polyubiqutin chains attached to CAV1 and compromise its activity in the lysosomal degradation of the TGF-β receptors.Regarding the functional consequences of POH1-mediated promotion of TGF-β signaling in HCC cells, we found that POH1 substantially increased the metastatic potential of HCC cells both in vitro and in vivo."

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"More importantly, the findings that POH1 promotes TGF-β signaling can be further demonstrated with clinical data."

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"Collectively, these results strongly suggest that POH1 may promote TGF-β signaling in HCC.Consistently, Kaplan-Meier analyses from the HCC samples revealed that the patients with higher staining scores of POH1 and p-SMAD3 had lower overall survival (Fig. 2c) and more advanced progression (Fig. 2d)."

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"Knockdown of miR-378 or overexpression of PSMD14 reduced the protective effects of ucMSC-EVs by activating the TGF-β1/Smad2/3 signaling pathway."

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"To understand how POH1 positively regulates TGF-β signaling, we performed high-throughput liquid chromatography-mass spectrometry (LC-MS/MS) analyses to identify the proteins potentially interacting with POH1."

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"This finding led us to hypothesize that increased TGF-β signaling by POH1 may be directly attributed to POH1 regulation of TGF-β receptor abundance."