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Biology subjects

Wang, L.-T.

Publications and source records attributed to Wang, L.-T..

2 recordsLinked to original sources

Ellagic acid ameliorates atherosclerosis by targeting the epidermal growth factor receptor

BACKGROUNDHigh levels of plasma low-density lipoprotein (LDL) are a key risk factor for atherosclerosis. Low-density lipoprotein receptor (LDLR) mediates the degradation of plasma LDL. Therefore, it may be possible to prevent and treat atherosclerosis by increasing the levels of LDLR. The natural polyphenolic compound ellagic acid (EA) has various biological activities. In mice, EA alleviated the progression of atherosclerosis; however, the underlying mechanism remains unclear. METHODSMolecular interaction, cell, and animal experiments were used to explore the role and mechanism of EA in improving atherosclerosis. RESULTSEA binds to the extracellular domain of the epidermal growth factor receptor (EGFR), thus activating the EGFR-extracellular signal-regulated kinase (EGFR-ERK) signaling pathway, stabilizing LDLR mRNA, and promoting the expression of LDLR protein. The development of EA-loaded human serum albumin nanoparticles enabled intravenous administration in animal experiments. CONCLUSIONSThe research verified the in vivo effects of EA on the EGFR-ERK signaling pathway, LDLR levels, and atherosclerosis. EA may assist in the prevention and treatment of atherosclerosis.

biochemistry↗

Girdin is a component of the lateral polarity protein network restricting cell dissemination

Epithelial cell polarity defects support cancer progression. It is thus crucial to decipher the functional interactions within the polarity protein network. Here we show that Drosophila Girdin and its human ortholog (GIRDIN) sustain the function of crucial lateral polarity proteins by inhibiting the apical kinase aPKC. Loss of GIRDIN expression is also associated with overgrowth of disorganized cell cysts. Moreover, we observed cell dissemination from GIRDIN knockdown cysts and tumorspheres, thereby showing that GIRDIN supports the cohesion of multicellular epithelial structures. Consistent with these observations, alteration of GIRDIN expression is associated with a poor overall survival in subtypes of breast and lung cancers. Overall, we discovered a core mechanism contributing to epithelial cell polarization from flies to humans. Our data also indicate that GIRDIN has the potential to impair the progression of epithelial cancers by preserving cell polarity and restricting cell dissemination.

cell biology↗