{"title":"Effect of silencing of GRHL2 on proliferation and apoptosis of lung cancer A549 cells","authors":"Mingli Wei, N. Huang","doi":"10.3760/CMA.J.CN131368-20190524-00774","DOIUrl":null,"url":null,"abstract":"Objective \nTo investigate the effect of GRHL2 silencing on proliferation and apoptosis of lung cancer A549 cells. \n \n \nMethods \nUsing RNA interference technology, the expression vector of GRHL2 silenced lentivirus was constructed to infect lung cancer A549 cells, the experiment was divided into the experimental group (GRHL2 silences the A549 cell line infected by lentivirus), the negative control group (the A549 cell line infected by no-load lentivirus), the blank control group (the A549 cell line without any treatment). The intensity of green fluorescent protein was observed by inverted fluorescence microscope, and the expression levels of GRHL2 mRNA and protein in lung cancer A549 cells were detected by quantitative real-time polymerase chain reaction and Western blot.Cell counting kit-8 was used to detect the effect of GRHL2 silencing on A549 cell proliferation.Annexin V-APC /PI reagents and flow analysis were used to analyze the effect of GRHL2 silencing on the apoptosis of A549 cells. \n \n \nResults \nThe expression levels of GRHL2 mRNA and protein in the experimental group were significantly decreased than the negative control groupand blank control group (F=48.13, 42.57, both P<0.05), the proliferation ability of A549 cells was significantly decreased (F=65.64, P<0.05), and apoptosis was significantly increased (F=56.76, P<0.05). \n \n \nConclusions \nTargeted silencing of GRHL2 can significantly inhibit the proliferation and promote apoptosis of lung cancer A549 cells, and GRHL2 is expected to become a new target for clinical lung cancer targeted therapy. \n \n \nKey words: \nLentivirus infections; Cell proliferation; Apoptosis; GRHL2; A549","PeriodicalId":10004,"journal":{"name":"Chinese Journal of Asthma","volume":"32 2 1","pages":"481-486"},"PeriodicalIF":0.0000,"publicationDate":"2020-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Chinese Journal of Asthma","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3760/CMA.J.CN131368-20190524-00774","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Objective
To investigate the effect of GRHL2 silencing on proliferation and apoptosis of lung cancer A549 cells.
Methods
Using RNA interference technology, the expression vector of GRHL2 silenced lentivirus was constructed to infect lung cancer A549 cells, the experiment was divided into the experimental group (GRHL2 silences the A549 cell line infected by lentivirus), the negative control group (the A549 cell line infected by no-load lentivirus), the blank control group (the A549 cell line without any treatment). The intensity of green fluorescent protein was observed by inverted fluorescence microscope, and the expression levels of GRHL2 mRNA and protein in lung cancer A549 cells were detected by quantitative real-time polymerase chain reaction and Western blot.Cell counting kit-8 was used to detect the effect of GRHL2 silencing on A549 cell proliferation.Annexin V-APC /PI reagents and flow analysis were used to analyze the effect of GRHL2 silencing on the apoptosis of A549 cells.
Results
The expression levels of GRHL2 mRNA and protein in the experimental group were significantly decreased than the negative control groupand blank control group (F=48.13, 42.57, both P<0.05), the proliferation ability of A549 cells was significantly decreased (F=65.64, P<0.05), and apoptosis was significantly increased (F=56.76, P<0.05).
Conclusions
Targeted silencing of GRHL2 can significantly inhibit the proliferation and promote apoptosis of lung cancer A549 cells, and GRHL2 is expected to become a new target for clinical lung cancer targeted therapy.
Key words:
Lentivirus infections; Cell proliferation; Apoptosis; GRHL2; A549