The integration of different imaging functions into an ultrasmall nanoplatform with excellent biocompatibility and metabolic performance to fabricate multimodal imaging probes has been a tremendous challenge. Herein, a novel kind of gadolinium-and ytterbium-doped carbon dots (Gd/Yb@ CDs) with diameter of 5.26 ± 0.93 nm was obtained by the convenient one-step hydrothermal process for magnetic resonance imaging (MRI), X-ray computed tomography (CT), and fluorescent imaging (FI). The obtained Gd/Yb@ CDs exhibited not only the excitation-dependent emission and superhigh photostability but also higher longitudinal relaxivity (r 1 = 6.65 mM −1 s −1 ) and excellent X-ray absorption performance (45.43 HU L g −1 ). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, tissue section assessment, and body weight investigation shed light on the superior biocompatibility of these Gd/Yb@CDs. MRI/CT imaging demonstrated these multimodal nanoprobes could give rise to obviously enhanced contrast effect on the xenografted tumor model. Furthermore, biodistribution analysis demonstrated that these nanoprobes could be easily removed from the mice through the kidney elimination pathway. Therefore, the present Gd/Yb@CDs could be served as promising MRI/CT/FI multimodal nanoprobes to provide more accurate and comprehensive diagnosis information.
Emerging evidence has indicated the important function of long non‐coding RNAs (lncRNAs) in tumour chemotherapy resistance. However, the underlying mechanism is still ambiguous. In this study, we investigate the physiopathologic role of lncRNA ferritin heavy chain 1 pseudogene 3 (FTH1P3) on the paclitaxel (PTX) resistance in breast cancer. Results showed that lncRNA FTH1P3 was up‐regulated in paclitaxel‐resistant breast cancer tissue and cells (MCF‐7/PTX and MDA‐MB‐231/PTX cells) compared with paclitaxel‐sensitive tissue and parental cell lines (MCF‐7, MDA‐MB‐231). Gain‐ and loss‐of‐function experiments revealed that FTH1P3 silencing decreased the 50% inhibitory concentration (IC50) value of paclitaxel and induced cell cycle arrest at G2/M phase, while FTH1P3‐enhanced expression exerted the opposite effects. In vivo, xenograft mice assay showed that FTH1P3 silencing suppressed the tumour growth of paclitaxel‐resistant breast cancer cells and ABCB1 protein expression. Bioinformatics tools and luciferase reporter assay validated that FTH1P3 promoted ABCB1 protein expression through targeting miR‐206, acting as a miRNA “sponge.” In summary, our results reveal the potential regulatory mechanism of FTH1P3 on breast cancer paclitaxel resistance through miR‐206/ABCB1, providing a novel insight for the breast cancer chemoresistance.
A sensitive fluorescent probe based on carbon dots has been synthesized by a one-pot hydrothermal method for the rapid detection of intracellular Fe2+.
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