Chi Young Jung1, So-Young Kim2, Chuhee Lee3. 1. Department of Internal Medicine, College of Medicine, Catholic University of Daegu, Daegu, Republic of Korea. 2. Department of Pharmacology, School of Medicine, Dongguk University, Gyeongju, Republic of Korea. 3. Department of Biochemistry and Molecular Biology, School of Medicine, Yeungnam University, Daegu, Republic of Korea chlee2@ynu.ac.kr.
Abstract
BACKGROUND/AIM: AXL has been reported to be overexpressed and highly activated in various cancer types. In this study, we demonstrated the effect of carvacrol on cell proliferation and migration in non-small cell lung cancer (NSCLC) cells by impeding the expression and activation of AXL. MATERIALS AND METHODS: The levels of AXL protein, mRNA and promoter activity were evaluated by western blot, reverse transcription polymerase chain reaction (RT-PCR) and luciferase assay, respectively. AXL-overexpressing cells were established by ectopic expression of AXL cDNA. Cell viability, clonogenicity, and migration were measured in carvacrol-treated NSCLC cells. RESULTS: Carvacrol treatment of NSCLC cells caused down-regulation of AXL expression at the transcriptional level and also inhibited phosphorylation of AXL upon ligand stimulation. Carvacrol suppressed cell proliferation and migration and its inhibitory effect was attenuated in AXL-overexpressing NSCLC cells. CONCLUSION: Our data demonstrate that AXL is a crucial therapeutic target of carvacrol-induced inhibition of NSCLC cell proliferation and migration. Copyright
BACKGROUND/AIM: AXL has been reported to be overexpressed and highly activated in various cancer types. In this study, we demonstrated the effect of carvacrol on cell proliferation and migration in non-small cell lung cancer (NSCLC) cells by impeding the expression and activation of AXL. MATERIALS AND METHODS: The levels of AXL protein, mRNA and promoter activity were evaluated by western blot, reverse transcription polymerase chain reaction (RT-PCR) and luciferase assay, respectively. AXL-overexpressing cells were established by ectopic expression of AXL cDNA. Cell viability, clonogenicity, and migration were measured in carvacrol-treated NSCLC cells. RESULTS:Carvacrol treatment of NSCLC cells caused down-regulation of AXL expression at the transcriptional level and also inhibited phosphorylation of AXL upon ligand stimulation. Carvacrol suppressed cell proliferation and migration and its inhibitory effect was attenuated in AXL-overexpressing NSCLC cells. CONCLUSION: Our data demonstrate that AXL is a crucial therapeutic target of carvacrol-induced inhibition of NSCLC cell proliferation and migration. Copyright
Authors: Thaíssa Q Machado; Anna C C da Fonseca; Allana B S Duarte; Bruno K Robbs; Damião P de Sousa Journal: Biomed Res Int Date: 2022-05-24 Impact factor: 3.246