Yujun Wang1,2, Lijuan Yu1, Tao Wang3. 1. Central of PET/CT-MR, Cancer Hospital Affiliated to Harbin Medical University, Harbin 150000, China. 2. Department of Nuclear Medicine, Hainan Provincial Cancer Hospital, Haikou 570311, China. 3. Research Institute of Medicine and Pharmacy, Qiqihar Medical University, Qiqihar 161006, China.
Abstract
BACKGROUND: MicroRNAs (miRNAs) are reportedly involved in various cancers. The present study aimed to investigate the role of miRNA-374b in cell viability, proliferation, apoptosis, and tumor formation in non-small cell lung cancer (NSCLC) in humans. METHODS: The expression level of miRNA-374b in blood and tumor tissues from NSCLC patients was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to assess the viability of NSCLC cells after transfection with miRNA-374b. Colony formation assay was performed to assess the proliferation of cells pretreated with miRNA-374b. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay was performed to determine the role of miRNA-374b in apoptosis in NSCLC cells. A tumor formation assay was performed to assess the effects of miRNA-374b on tumorigenesis in NSCLC. RESULTS: miRNA-374b was markedly downregulated in the blood and tumor tissues from NSCLC patients. Furthermore, overexpression of miRNA-374b markedly reduced the viability of NSCLC cells, but miRNA-374b inhibitor increased the viability of NSCLC cells compared with that in negative controls. Moreover, miRNA-374b decreased the number of colonies; however, its corresponding anti-miRNA oligonucleotide (AMO) markedly increased colony formation by NSCLC cells. Also, miRNA-374b promoted the apoptosis and inhibited tumor formation in NSCLC; however, this inhibition was reversed upon treatment with the AMO. Western blot analysis revealed that miRNA-374b regulates tumor progression through the p38/ERK signaling pathway by inhibiting JAM-2 in NSCLC. CONCLUSIONS: The present results indicate that miRNA-374b inhibits tumor growth and promotes apoptosis in NSCLC through the p38/ERK signaling pathway by targeting JAM-2.
BACKGROUND: MicroRNAs (miRNAs) are reportedly involved in various cancers. The present study aimed to investigate the role of miRNA-374b in cell viability, proliferation, apoptosis, and tumor formation in non-small cell lung cancer (NSCLC) in humans. METHODS: The expression level of miRNA-374b in blood and tumor tissues from NSCLC patients was analyzed by quantitative reverse transcription polymerase chain reaction (qRT-PCR). A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to assess the viability of NSCLC cells after transfection with miRNA-374b. Colony formation assay was performed to assess the proliferation of cells pretreated with miRNA-374b. The terminal deoxynucleotidyl transferase-dUTP nick-end labeling (TUNEL) assay was performed to determine the role of miRNA-374b in apoptosis in NSCLC cells. A tumor formation assay was performed to assess the effects of miRNA-374b on tumorigenesis in NSCLC. RESULTS: miRNA-374b was markedly downregulated in the blood and tumor tissues from NSCLC patients. Furthermore, overexpression of miRNA-374b markedly reduced the viability of NSCLC cells, but miRNA-374b inhibitor increased the viability of NSCLC cells compared with that in negative controls. Moreover, miRNA-374b decreased the number of colonies; however, its corresponding anti-miRNA oligonucleotide (AMO) markedly increased colony formation by NSCLC cells. Also, miRNA-374b promoted the apoptosis and inhibited tumor formation in NSCLC; however, this inhibition was reversed upon treatment with the AMO. Western blot analysis revealed that miRNA-374b regulates tumor progression through the p38/ERK signaling pathway by inhibiting JAM-2 in NSCLC. CONCLUSIONS: The present results indicate that miRNA-374b inhibits tumor growth and promotes apoptosis in NSCLC through the p38/ERK signaling pathway by targeting JAM-2.
Authors: Hongxia Hao; Zhiguo Zhou; Shulong Li; Genevieve Maquilan; Michael R Folkert; Puneeth Iyengar; Kenneth D Westover; Kevin Albuquerque; Fang Liu; Hak Choy; Robert Timmerman; Lin Yang; Jing Wang Journal: Phys Med Biol Date: 2018-05-02 Impact factor: 3.609