Journal of translational medicine · 2014
Regulatory mechanisms of betacellulin in CXCL8 production from lung cancer cells.
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Shi Lin, Wang Lingyan, Wang Beibei, Cretoiu Sanda Maria, Wang Qun, Wang Xiangdong, Chen Chengshui
Аннотация
BACKGROUND: Betacellulin (BTC), a member of the epidermal growth factor (EGF) family, binds and activates ErbB1 and ErbB4 homodimers. BTC was expressed in tumors and involved in tumor growth progression. CXCL8 (interleukin-8) was involved in tumor cell proliferation via the transactivation of the epidermal growth factor receptor (EGFR).
MATERIALS AND METHODS: The present study was designed to investigate the possible interrelation between BTC and CXCL8 in human lung cancer cells (A549) and demonstrated the mechanisms of intracellular signals in the regulation of both functions. Bio-behaviors of A549 were assessed using Cell-IQ Alive Image Monitoring System.
RESULTS: We found that BTC significantly increased the production of CXCL8 through the activation of the EGFR-PI3K/Akt-Erk signal pathway. BTC induced the resistance of human lung cancer cells to TNF-α/CHX-induced apoptosis. Treatments with PI3K inhibitors, Erk1/2 inhibitor, or Erlotinib significantly inhibited BTC-induced CXCL8 production and cell proliferation and movement.
CONCLUSION: Our data indicated that CXCL8 production from lung cancer cells could be initiated by an autocrine mechanism or external sources of BTC through the EGFR-PI3K-Akt-Erk pathway to the formation of inflammatory microenvironment. BTC may act as a potential target to monitor and improve the development of lung cancer inflammation.
MATERIALS AND METHODS: The present study was designed to investigate the possible interrelation between BTC and CXCL8 in human lung cancer cells (A549) and demonstrated the mechanisms of intracellular signals in the regulation of both functions. Bio-behaviors of A549 were assessed using Cell-IQ Alive Image Monitoring System.
RESULTS: We found that BTC significantly increased the production of CXCL8 through the activation of the EGFR-PI3K/Akt-Erk signal pathway. BTC induced the resistance of human lung cancer cells to TNF-α/CHX-induced apoptosis. Treatments with PI3K inhibitors, Erk1/2 inhibitor, or Erlotinib significantly inhibited BTC-induced CXCL8 production and cell proliferation and movement.
CONCLUSION: Our data indicated that CXCL8 production from lung cancer cells could be initiated by an autocrine mechanism or external sources of BTC through the EGFR-PI3K-Akt-Erk pathway to the formation of inflammatory microenvironment. BTC may act as a potential target to monitor and improve the development of lung cancer inflammation.
Предметные рубрики MeSH
ApoptosisBetacellulinCell CountCell DifferentiationCell Line, TumorCell MovementCycloheximideDrug Resistance, NeoplasmErlotinib HydrochlorideExtracellular Signal-Regulated MAP KinasesHumansIntercellular Signaling Peptides and ProteinsInterleukin-8LipopolysaccharidesLung NeoplasmsModels, BiologicalPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsQuinazolinesReceptor Protein-Tyrosine KinasesTumor Necrosis Factor-alpha