Particulate matter 2.5 could induce DNA damage and cell senescence in corneal epithelial cells, probably by promoting ROS formation. Thus, whether long-term exposure of PM2.5 might be related to potential risk of abnormality in corneal epithelium renewal and regeneration should be further investigated.
The performance of graphene field effect transistors
(GFETs) strongly
depends on the interface between graphene sheets and the underlying
substrates. In this work, we report that an octadecyltrimethoxysilane
(OTMS) SAM modified conventional SiO2/Si substrate can
consistently enhance the performance of coronene-derived large-area
graphene FETs. The improved transport properties in terms of boosted
carrier mobility (up to 10 700 ± 300 cm2 V–1 s–1), long mean free path, nearly
vanished hysteretic behavior, and remarkably low intrinsic doping
level are mainly attributed to the strong suppression of interfacial
charge impurity scattering and remote interfacial phonon (RIP) scattering,
less adsorption of dipolar adsorbates, and the attenuated charger
transfer at the interface of graphene and dielectric. The intrinsic
doping levels (the Fermi energy) of graphene on OTMS-modified and
bare SiO2 have been quantitatively estimated and confirmed
by the Dirac points of GFETs, the Raman mapping of G-peak positions, and the surface potential maps by KPFM. The facile
fabrication of a graphene device over a large area provides an unprecedented
combination of high performance and low cost for the future application
of all carbon-based nanoelectronics.
Protein kinase C ε (PKCε) has emerged as an oncogenic protein kinase and plays important roles in cancer cell survival, proliferation, and invasion. It is, however, still unknown whether PKCε affects cell proliferation via glucose metabolism in cancer cells. Here we report a novel function of PKCε that provides growth advantages for cancer cells by enhancing tumor cells glycolysis. We found that either PKCε or Smad2/3 promoted aerobic glycolysis, expression of the glycolytic genes encoding HIF-1α, HKII, PFKP and MCT4, and tumor cell proliferation, while overexpression of PKCε or Smad3 enhanced aerobic glycolysis and cell proliferation in a protein kinase D- or TGF-β-independent manner in PC-3M and DU145 prostate cancer cells. The effects of PKCε silencing were reversed by ectopic expression of Smad3. PKCε or Smad3 ectopic expression-induced increase in cell growth was antagonized by inhibition of lactate transportation. Furthermore, interaction of endogenous PKCε with Smad2/3 was primarily responsible for phosphorylation of Ser213 in the Samd3 linker region, and resulted in Smad3 binding to the promoter of the glycolytic genes, thereby promoting cell proliferation. Forced expression of mutant Smad3 (S213A) attenuated PKCε-stimulated protein overexpression of the glycolytic genes. Thus, our results demonstrate a novel PKCε function that promotes cell growth in prostate cancer cells by increasing aerobic glycolysis through crosstalk between PKCε and Smad2/3.
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