Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

<p>Abstract</p> <p>Background</p> <p>To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.</p> <p>Methods</p> <p>MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR.</p> <p>Results</p> <p>HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased.</p> <p>Conclusions</p> <p>Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.</p

Hepatitis B virus induces G1 phase arrest by regulating cell cycle genes in HepG2.2.15 cells

<p>Abstract</p> <p>Background</p> <p>To investigate the effect of HBV on the proliferative ability of host cells and explore the potential mechanism.</p> <p>Methods</p> <p>MTT, colony formation assay and tumourigenicity in nude mice were performed to investigate the effect of HBV on the proliferative capability of host cells. In order to explore the potential mechanism, cell cycle and apoptosis were analysed. The cell cycle genes controlling the G1/S phase transition were detected by immunohistochemistry, westernblot and RT-PCR.</p> <p>Results</p> <p>HepG2.2.15 cells showed decreased proliferation ability compared to HepG2 cells. G1 phase arrest was the main cause but was not associated with apoptosis. p53, p21 and total retinoblastoma (Rb) were determined to be up-regulated, whereas cyclinE was down-regulated at both the protein and mRNA levels in HepG2.2.15 cells. The phosphorylated Rb in HepG2.2.15 cells was decreased.</p> <p>Conclusions</p> <p>Our results suggested that HBV inhibited the capability of proliferation of HepG2.2.15 cells by regulating cell cycle genes expression and inducing G1 arrest.</p

Oxygen Defect Engineering toward Zero-Strain V₂O_2.8@Porous Reticular Carbon for Ultrastable Potassium Storage

Potassium-ion batteries (KIBs) are promising candidates for large-scale energy storage devices due to their high energy density and low cost. However, the large potassium-ion radius leads to its sluggish diffusion kinetics during intercalation into the lattice of the electrode material, resulting in electrode pulverization and poor cycle stability. Herein, vanadium trioxide anodes with different oxygen vacancy concentrations (V2O2.9, V2O2.8, and V2O2.7 determined by the neutron diffraction) are developed for KIBs. The V2O2.8 anode is optimal and exhibits excellent potassium storage performance due to the realization of expanded interlayer spacing and efficient ion/electron transport. In situ X-ray diffraction indicates that V2O2.8 is a zero-strain anode with a volumetric strain of 0.28% during the charge/discharge process. Density functional theory calculations show that the impacts of oxygen defects are embodied in reducing the band gap, increasing electron transfer ability, and lowering the diffusion energy barriers for potassium ions. As a result, the electrode of nanosized V2O2.8 embedded in porous reticular carbon (V2O2.8@PRC) delivers high reversible capacity (362 mAh g–1 at 0.05 A g–1), ultralong cycling stability (98.8% capacity retention after 3000 cycles at 2 A g–1), and superior pouch-type full-cell performance (221 mAh g–1 at 0.05 A g–1). This work presents an oxygen defect engineering strategy for ultrastable KIBs