ABSTRACT
Objective: To investigate the molecular mechanism of isofebrifuzine in the treatment of esophageal cancer by observing the effects of isofebrifuzine on proliferation, apoptosis, cycle, energy metabolism and protein expression related to energy metabolism pathway in EC9706 cells. Methods: ECC9706 cells were routinely cultured, cell activity was detected by MTT method, drug concentration was screened, and two concentrations of 1 μg/mL and 2 μg/mL were selected, the effect of isofebrifuzine on apoptosis and cycle of esophageal cancer cells EC9706 was detected by flow cytometry. The effect of isofebrifuzine on energy metabolism of EC9706 cells was detected by energy metabolism detection system, and the protein expressions of mTOR, p-mTOR, p-ACC and AMPK in cells were detected by Western blotting. Results: The proliferation of EC9706 cells was effectively inhibited in a dose-dependent manner (P < 0.01) after 48 h of treatment with different concentrations of isofebrifuzine, which could arrest EC9706 cells in S phase and G2/M phase (P < 0.05), effectively promote cell apoptosis (P < 0.05), and significantly inhibit cell glycolysis and mitochondrial metabolism (P < 0.01). Compared with the control group, AMPK expression was increased and mTOR, p-mTOR, p-ACC expression was decreased in the treatment group (P < 0.05). Conclusion: These results indicated that isofebrifuzine may regulate the cycle and apoptosis of EC9706 cells and inhibit the proliferation of EC9706 cells in esophageal cancer through energy metabolism.
ABSTRACT
Aim To investigate the influence of inhibi-tory nanocomposite on EC-9706 cells and the effect of nanocomposite on ESCCAL _ 1 LncRNA expression, siRNA-loaded nanocomposite being prepared as non-vi-rus delivery system Methods Mesoporous silica nano-particles were prepared by sol-gel method under room temperature and coated by cationic polymerpolyethylen-imine (PEI)on the surface to stay positive charge, which could facilitate its combination with negatively charged ESCCAL _ 1 siRNA. The size and surface charge of nanocomposite were determined by laser par-ticle analyzer and TEM. The inhibitory rate of nanopar-ticles on EC-9706 cells was detected by MTT methods. Entrapment efficiency was determined by agarose gel e-lectrophoresis. The uptake-siRNA was detected by flu-orescence microscope. The expression of ESCCAL _1 LncRNA was detected by RT-PCR. Results The MSNP appeared to have a high dispensability and hom-ogeneous size by particle size analyzer and transmission electron microscopy(TEM). The formed nanoparticles had a surface mesoporous diameter of 3 ~ 5 nm. The proliferation of ESCCAL_1 was inhibited significantlly (P < 0. 05),and the 72h inhibitory rate was (54. 93 ± 2. 6)%;the siRNA loading could be effectively up-taken by EC-9706 cells;ESCCAL_1 silencing efficien-cy was 69. 5% . Conclusions The tumor targeting nanocomposite with high encapsulation efficiency is prepared. The proliferation of esophageal cancer EC-9706 cells can be effectively inhibited by anocompos-ite-mediated siRNA,and the expression of ESCCAL_1 is effectively silenced in EC-9706 cells. The nanocom-posite is an efficient gene delivery system and may have potential application in gene therapy.
ABSTRACT
Aim To study the mechanism of andrographolide(AD) on the proliferation and apoptosis induction in human esophageal cancer Ec9706 cells.Methods The spectrometry was used to detect the activity of caspase-3 in human esophageal cancer Ec9706 cells treated with or without AD for 6 h,12 h and 18 h,and to detect the activity of caspase-8 and caspase-9 in human esophageal cancer Ec9706 cells treated with or without AD for 6 h.The influence of AD on the proliferation of Ec9706 cells after treatment with or without Z-VAD-FMK(a broad-spectrum caspase inhibitor) was determined by MTT method and the result was compared.The changes of gene expression levels of bcl-2 were determined by immunohistochemical method.Results The expression level of bcl-2 gene was obviously lower in the cells treated with AD(30 mg?L-1,P