Herein, we report
on a two-dimensional amino-functionalized Ti3C2-MXene (N–Ti3C2-MXene)-based
surface plasmon resonance (SPR) biosensor for detecting carcinoembryonic
antigen (CEA) utilizing a sandwich format signal amplification strategy.
Our biosensor employs an N-Ti3C2-MXene nanosheet-modified
sensing platform and a signal enhancer comprising N-Ti3C2-MXene-hollow gold nanoparticles (HGNPs)-staphylococcal
protein A (SPA) complexes. Ultrathin Ti3C2-MXene
nanosheets were synthesized and functionalized with aminosilane to
provide a hydrophilic-biocompatible nanoplatform for covalent immobilization
of the monoclonal anti-CEA capture antibody (Ab1). The
N-Ti3C2-MXene/HGNPs nanohybrids were synthesized
and further decorated with SPA to immobilize the polyclonal anti-CEA
detection antibody (Ab2) and serve as signal enhancers.
The capture of CEA followed by the formation of the Ab2-conjugated SPA/HGNPs/N-Ti3C2-MXene sandwiched
nanocomplex on the SPR chip results in the generation of a response
signal. The fabricated N-Ti3C2-MXene-based SPR
biosensor exhibited a linear detection range of 0.001–1000
PM with a detection limit of 0.15 fM. The proposed biosensor showed
high sensitivity and specificity for CEA in serum samples, which gives
it application potential in the early diagnosis and monitoring of
cancer. We believe that this work also opens new avenues for development
of MXene-based highly sensitive biosensors for determining various
biomolecules.
Liver fibrosis results from a sustained wound healing response to chronic liver injury, and the activation of nonparenchymal hepatic stellate cells (HSCs) is the pivotal process. MicroRNA-34a (miR-34a) is the direct target gene of p53 and activates p53 through sirtuin 1 (SIRT1) simultaneously. The miR-34a/SIRT1/p53 signaling pathway thus forms a positive feedback loop wherein p53 induces miR-34a and miR-34a activates p53 by inhibiting SIRT1, playing an important role in cell proliferation and apoptosis. miR-34a expression has been found to be increased in animal models or in human patients with different liver diseases, including liver fibrosis. However, the exact role of this classical miR-34a/SIRT1/p53 signaling pathway in liver fibrosis remains unclear. In the present study, using a CCl4-induced rat liver fibrosis model, we found that the miR-34a/SIRT1/p53 signaling pathway was activated and could be inhibited by SIRT1 activator SRT1720. Further studies showed that the miR-34a/SIRT1/p53 signaling pathway was activated in hepatocytes but not in HSCs. The activation of this pathway in hepatocytes resulted in the apoptosis of hepatocytes and thus activated HSCs. Our data indicate that the miR-34a/SIRT1/p53 signaling pathway might be a promising therapeutic target for liver fibrosis.
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