Abstract：
:Inflammatory stimuli clearly contribute to lung cancer development and progression, but the underlying pathogenic mechanisms are not fully understood. We found that the proinflammatory cytokine IL-1β is dramatically elevated in the serum of patients with non-small cell lung cancer (NSCLC). In vitro studies showed that IL-1β promoted the proliferation and migration of NSCLC cells. Mechanistically, IL-1β acted through the COX2-HIF1α pathway to repress the expression of microRNA-101 (miR-101), a microRNA with an established role in tumor suppression. Lin28B was identified as critical effector target of miR-101 with its repression of Lin28B, a critical aspect of tumor suppression. Overall, IL-1β upregulated Lin28B by downregulating miR-101. Interestingly, cyclooxygenase-2 inhibition by aspirin or celecoxib abrogated IL-1β-mediated repression of miR-101 and IL-1β-mediated activation of Lin28B along with their stimulatory effects on NSCLC cell proliferation and migration. Together, our findings defined an IL-1β-miR-101-Lin28B pathway as a novel regulatory axis of pathogenic inflammatory signaling in NSCLC.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Wang L,Zhang LF,Wu J,Xu SJ,Xu YY,Li D,Lou JT,Liu MFdoi
10.1158/0008-5472.CAN-14-0960subject
Has Abstractpub_date
2014-09-01 00:00:00pages
4720-30issue
17eissn
0008-5472issn
1538-7445pii
0008-5472.CAN-14-0960journal_volume
74pub_type
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