Different rabies virus (RABV) strains have their own biological characteristics, but little is known about their respective impact on autophagy. Therefore, we evaluated whether attenuated RABV HEP-Flury and wildtype RABV GD-SH-01 strains triggered autophagy. We found that GD-SH-01 infection significantly increased the number of autophagy-like vesicles, the accumulation of enhanced green fluorescent protein (EGFP)-LC3 fluorescence puncta and the conversion of LC3-I to LC3-II, while HEP-Flury was not able to induce this phenomenon. When evaluating autophagic flux, we found that GD-SH-01 infection triggers a complete autophagic response in the human neuroblastoma cell line (SK), while autophagosome fusion with lysosomes was inhibited in a mouse neuroblastoma cell line (NA). In these cells, GD-SH-01 led to apoptosis and mitochondrial dysfunction while triggering autophagy, and apoptosis could be decreased by enhancing autophagy. To further identify the virus constituent causing autophagy, 5 chimeric recombinant viruses carrying single genes of HEP-Flury instead of those of GD-SH-01 were rescued. While the HEP-Flury virus carrying the wild-type matrix protein (M) gene of RABV triggered LC3-I to LC3-II conversion in SK and NA cells, replacement of genes of nucleoprotein (N), phosphoprotein (P) and glycoprotein (G) produced only minor autophagy. But no one single structural protein of GD-SH-01 induced autophagy. Moreover, the AMPK signaling pathway was activated by GD-SH-01 in SK. Therefore, our data provide strong evidence that autophagy is induced by GD-SH-01 and can decrease apoptosis in vitro. Furthermore, the M gene of GD-SH-01 may cooperatively induce autophagy.
Lung cancer is among the most common malignant tumors worldwide, and is characterized by a low survival rate compared with other cancers. Toll-like receptors (TLRs) are highly conserved in evolution and widely expressed on immune cells, where they serve an important role in the innate immune system by evoking inflammatory responses. Evasion of immune destruction is an important hallmark in the development of cancer. There is an established association between chronic inflammation and cancer, with TLRs serving important roles in the immune response against tumor cells. Recently, TLRs have been identified on tumor cells, where their activation may orchestrate the downstream signaling pathways that serve crucial functions in tumorigenesis and tumor progression. The present review summarizes the roles of TLRs as sensors on lung cancer cells that regulate lung cancer progression with regard to cell growth and invasion, angiogenesis and cancer stem cell behavior. This aimed to provide theoretical support for the development of therapies that target TLR signaling pathways for the treatment of lung cancer.
A simple and mild protocol for copper catalyzed halogenation of quinoline at C5 and C7 positions was developed, affording the desired remote C-H activation products in moderate to good yields. This reaction proceeds with low-cost sodium halides (NaX, X = Cl, Br, I) and features excellent substrate tolerance. A series of control experiments were carried out to illustrate a single-electron-transfer process which plays a vital role in the halogenation.
The kinetics of acid deprotonation on the Cu(100) surface have been studied using four different fluorinated carboxylic acids (CF2HCO2H, CF3CO2H, CF2HCF2CO2H, and CF3CF2CO2H). All four acids adsorb molecularly on Cu(100) at 90 K but deprotonate during heating to form carboxylates on the surface at temperatures below 300 K. Temperature-programmed reaction spectroscopy and X-ray photoemission spectroscopy were used to verify that the acids deprotonate on the Cu(100) surface. Work function measurements were used to study the deprotonation kinetics during heating and to estimate the activation energy barriers ( ) to deprotonation. The nature of the transition state to acid deprotonation on Cu(100) was probed by analysis of linear free energy relationships (LFER) or correlations of with the acid substituent constants, σF. The field reaction constant, ρF, or the slope of the LFER was found to be ρF = −52 ± 13 kJ/mol in the limit of zero coverage and ρF = −19 ± 2 kJ/mol at a coverage of 1/2 ML. These values of ρF can be compared to the value of ρF = −104 kJ/mol for acid deprotonation in the gas phase. This comparison suggests that the transition state for acid deprotonation on Cu(100) must be anionic with respect to the reactant (RCO2H(ad) ↔ [RCO2 δ-···Hδ+]‡ → ).
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