ABSTRACT
OBJECTIVE: To study the effect of miR-16-5p on lung cancer cell injury and apoptosis, and its mechanism. METHODS: LPS induced lung cancer cell A549 injury; qRT-PCR method was applied to detect the expression of miR-16-5p and CXCR3 in A549 cells. Con (without LPS treatment), LPS + miR-NC group (transfected negative control samples), LPS + miR-16-5p group (transfected miR-16-5p mimics); LPS + si-NC group (transfected negative control samples), LPS + si-CXCR3 group (transfected si-CXCR3); LPS + miR-16-5p + pcDNA3.1 group (co-transfected miR-16-5p mimics and pcDNA3.1), LPS + miR-16-5p + pcDNA3.1-CXCR3 group (co-transfected miR-16-5p mimics and pcDNA3.1-CXCR3) were transfected into A549 cells by liposome method. Western blot was used to detect protein expression of CXCR3, IL-6 and TNF-α in A549 cells; apoptosis of A549 cells was detected by flow cytometry. RESULTS: Compared with the control group, the expression of miR-16-5p mRNA was significantly decreased in A549 cells in LPS group, and the mRNA and protein expression of CXCR3 were significantly increased (p < .05). Overexpression of miR-16-5p and knockdown of CXCR3 both can down-regulated protein expression of IL-6 and TNF-α, and up-regulated apoptosis in LPS-induced A549 cell; CXCR3 is a target of miR-16-5p. Overexpression of CXCR3 rescued the protective effect of miR-16-5p on LPS-induced A549 cell injury. CONCLUSION: miR-16-5p can protect LPS-induced A549 cell injury, and its mechanism may be related to the targeted regulation of CXCR3, which could provide a new target for targeted therapy of lung cancer.
Subject(s)
Lipopolysaccharides/pharmacology , MicroRNAs/genetics , Receptors, CXCR3/genetics , A549 Cells , Apoptosis/drug effects , Apoptosis/genetics , Base Sequence , Gene Expression Regulation, Neoplastic/drug effects , Gene Expression Regulation, Neoplastic/genetics , Gene Knockdown Techniques , Humans , Interleukin-6/genetics , Receptors, CXCR3/deficiency , Tumor Necrosis Factor-alpha/geneticsABSTRACT
OBJECTIVE: To study the effect of microRNA-1224 (miR-1224) on hydrogen peroxide (H2 O 2 )-induced oxidative stress injury in hepatocytes, and explore its underlying mechanism. METHODS: L02 cells were treated with H2 O 2 (100 mmol/L) to establish the model of an oxidative stress injury in hepatocytes. Quantitative reverse transcriptase polymerase chain reaction was used to detect the expression of miR-1224 and hepatocyte growth factor (HGF) in L02 cells. L02 cells were transfected with anti-miR-con (H 2 O 2 + anti-miR-con group), anti-miR-1224 (H 2 O 2 + anti-miR-1224 group), pcDNA3.1 (H 2 O 2 + ctrl group), pcDNA3.1-HGF (H 2 O 2 + HGF group), si-HGF and anti-miR-1224 (H 2 O 2 + anti-miR-1224 + HGF group), si-NC and anti-miR-1224 (H 2 O 2 + anti-miR-1224 + ctrl group) by liposome method. Cells without any treatment were regarded as a negative control (NC) group. The protein expression of HGF in each group cells was detected by Western blot analysis. Cell viability and apoptosis of each group were detected by 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assay or flow cytometry, respectively. The interaction between miR-1224 and HGF was measured by dual luciferase reporter gene assay. RESULTS: The expression of miR-1224 was enhanced in H2 O 2 -treated L02 cells and its knockdown alleviated H 2 O 2 -induced suppression of viability and promotion of apoptosis. HGF is a target of miR-1224 and its overexpression abated H 2 O 2 -induced injury in hepatocytes. Moreover, silencing of HGF rescued the effect of downregulation of miR-1224 on cell viability and apoptosis in H 2 O 2 -treated L02 cell. CONCLUSION: Downregulation of miR-1224 could attenuate oxidative stress-induced inhibition of viability and increase of apoptosis in hepatocytes by targeting HGF, which may provide a target for potential therapy of acute liver injury.
Subject(s)
Chemical and Drug Induced Liver Injury/prevention & control , Gene Expression Regulation , Hepatocytes/metabolism , Hydrogen Peroxide/toxicity , MicroRNAs/antagonists & inhibitors , Oxidative Stress , Protective Agents , Cell Proliferation , Chemical and Drug Induced Liver Injury/etiology , Chemical and Drug Induced Liver Injury/metabolism , Chemical and Drug Induced Liver Injury/pathology , Hepatocytes/cytology , Humans , Oxidants/toxicityABSTRACT
The new method of manufacturing individual mandibular prostheses, in combination with CT data and CNC technique, can duplicate bone tissues accurately, and can have the individual mandibular prosthesis made to order, and repair the mandibular defect (especially the lager mandibular segmental defect).
