In this paper, we first synthesis three-dimensional jasmine-like Cu@L-aspartic acid(L-ASP) inorganic–organic hybrid nanoflowers to load palladium-platinum nanoparticles (Pd–Pt NPs) as the signal enhancer in order to quantify intracellular speckle-type POZ domain protein. Scanning electron microscope, fourier transform infrared, energy dispersive spectrometer, X-ray photoelectron spectroscopy analysis was used to characterize the newly synthesized materials. The newly formed Cu@L-Asp/Pd-PtNPs can catalyze the decomposition of hydrogen peroxide and exhibit excellent catalytic performance. When different concentration of speckle-type POZ domain protein is captured by speckle-type POZ domain protein antibody linked to the surface of Cu@L-Asp/Pd–Pt NPs, the current signal decreases with the increase concentration of speckle-type POZ domain protein. After optimization, the speckle-type POZ domain protein immunosensor exhibited a good linear response over a concentration range from 0.1–1 ng mL −1 with a low detection limit of 19 fg mL −1 . The proposed sensor demonstrates good stability within 28 days, acceptable reproducibility (RSD = 0.52%) and selectivity to the speckle-type POZ domain protein in the presence of possible interfering substances and has potential application for detecting other intracellular macromolecular substances.
Tan Peng,Xu Yunke,Du Yichao,Wu Lile,Guo Bing,Huang Shiyao,Zhu Jinhui,Li Bo,Lin Fujun,Yao Lei
Speckle-type POZ domain protein (SPOP), an adaptor in the E3 ubiquitin ligase complex, recognizes substrates and promotes protein degradation via the ubiquitin-proteasome system. It appears to help regulate progression of several cancers, and we show here that it acts as a tumor suppressor in pancreatic cancer. Our analysis of patient tissues showed decreased SPOP expression, which was associated with poor prognosis. SPOP knockdown in SW1990 (in vitro/vivo) and PANC-1 (in vitro) cells led to significantly greater proliferation, migration, and invasion. Co-immunoprecipitation experiments in SW1990 cells showed that SPOP interacted with the stem-cell marker NANOG, and this interaction has recently been shown to play a critical role in regulating progression of prostate cancer. We showed that, in one patient with pancreatic cancer, the expression of a truncated form of SPOP (p.Q360*) lacking the nuclear localization signal led to nuclear accumulation of NANOG, which promoted growth and metastasis of pancreatic cancer cells. Our results suggest that SPOP suppresses progression of pancreatic cancer by promoting the ubiquitination and subsequent degradation of NANOG. These results identify the SPOP-NANOG interaction as a potential therapeutic target against pancreatic cancer.
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