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Feng, S.-S.

Publications and source records attributed to Feng, S.-S..

2 recordsLinked to original sources

Planting graphene quantum dots in PEGylated nanoparticles for enhanced and multimodal in vivo imaging of tumor

Photoluminescent graphene quantum dots (GQDs) have recently attracted considerable attention for biomedical applications owing to the interesting physicochemical and photophysical properties, and prominent biocompatibility and biosafety. However, although much progress has been achieved in therapy and in vitro bioimaging, broad and crucial in vivo fluorescence bioimaging and synergistically working with other nanomedicine are very challenging and limited. Herein, we in situ implanted GQDs in the PEGylated layer of nanoparticles (NPs) via a bottom-up approach to obtain the NPs (core)-GQDs-PEG multifunctional nanoprobe (NPC-GQDs-PEG), which prolonged the blood circulation of GQDs more than four times and increased the tumor accumulation 7~8 times than GQDs used alone. Under assisted by the flexible microscope, the GQDs were successfully used for in vivo real-time monitoring of local NPs pharmacokinetics, in vivo multimodality imaging, and fluorescence imaging-guided tumor surgery. The approach of implanting GQDs in PEGylated nanomedicine and synergistic working provide a new strategy for in vivo biomedical applications of GQDs.

cancer biology↗

LncRNA GUARDIN suppresses cellular senescence through a LRP130-PGC1α-FOXO4-p21-dependent signaling axis

The long non-coding RNA GUARDIN functions to protect genome stability. Inhibiting GUARDIN expression can alter cell fate decisions towards senescence or apoptosis, but the underlying molecular signals are unknown. Here we show that GUARDIN is an essential component of a transcriptional repressor complex involving LRP130 and PGC1 which suppresses FOXO4 expression. GUARDIN acts as a scaffold to stabilize LRP130/PGC1 heterodimers and their occupancy at the FOXO4 promotor. Destabilizing this complex by silencing of GUARDIN, LRP130 or PGC1 leads to FOXO4-dependent upregulation of p21, thereby driving cells into senescence. We also found that GUARDIN expression was induced by rapamycin, a senolytic agent that suppresses cell senescence. FOS-Like Antigen 2 (FOSL2) acts as a transcriptional repressor of GUARDIN with increased levels in the presence of rapamycin resulting from downregulation of FOSL2. Together, these results demonstrate that GUARDIN inhibits p21-dependent senescence through a LRP130-PGC1-FOXO4 signaling axis and moreover, GUARDIN contributes to the anti-senolytic activities of rapamycin.

cell biology↗