title: miR-214 promotes tumorigenesis by targeting lactotransferrin in nasopharyngeal carcinoma.
abstract: LTF (lactotransferrin, or lactoferrin) plays important role in innate immunity, and its anti-tumor function has also been reported in multiple cancers. We previously reported that LTF is significantly down-regulated in nasopharyngeal carcinoma (NPC) and acts as a tumor suppressor by suppressing AKT signaling. However, the exact mechanism of the down-regulation of LTF in NPC has not been revealed. In the current study, we screened and identified LTF is a bona fide target of miR-214 in NPC cells. miR-214 mimics significantly suppressed LTF mRNA and protein expression levels in NPC cells. miR-214 not only can promote NPC cell proliferation and invasion abilities in vitro, but also can accelerate tumor formation and lung metastasis in a mouse xenograft model. The pro-tumor function of miR-214 was depended on LTF suppression since LTF re-expression can reverse it. miR-214 can also activate AKT signaling by suppressing LTF expression. Furthermore, miR-214 expression level was up-regulated in NPC especially in metastasis-prone NPC tumor tissues compared with normal nasopharyngeal epithelial tissues, while the LTF expression level was negatively correlated with miR-214, suggesting that miR-214 targeting is partly responsible for LTF down-regulation in NPC specimens.
authors.affiliation: Cancer Research Institute, Central South University, Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Changsha, China.
authors.forename: Min
authors.initials: M
authors.lastname: Deng
authors.forename: Qiurong
authors.initials: Q
authors.lastname: Ye
authors.forename: Zailong
authors.initials: Z
authors.lastname: Qin
authors.forename: Ying
authors.initials: Y
authors.lastname: Zheng
authors.forename: Wei
authors.initials: W
authors.lastname: He
authors.forename: Hailin
authors.initials: H
authors.lastname: Tang
authors.forename: Yanhong
authors.initials: Y
authors.lastname: Zhou
authors.forename: Wei
authors.initials: W
authors.lastname: Xiong
authors.forename: Ming
authors.initials: M
authors.lastname: Zhou
authors.forename: Xiaoling
authors.initials: X
authors.lastname: Li
authors.forename: Qun
authors.initials: Q
authors.lastname: Yan
authors.forename: Jian
authors.initials: J
authors.lastname: Ma
authors.forename: Guiyuan
authors.initials: G
authors.lastname: Li
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D016022:Case-Control Studies; D002465:Cell Movement; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D002478:Cells, Cultured; D015536:Down-Regulation; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D007124:Immunoenzyme Techniques; D007781:Lactoferrin / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D008156:Luciferases / Q000378:metabolism; D008207:Lymphatic Metastasis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism; D008875:Middle Aged; D009303:Nasopharyngeal Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D009305:Nasopharynx / Q000378:metabolism* / Q000473:pathology; D009367:Neoplasm Staging; D011379:Prognosis; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: C547397:MIRN214 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; D008156:Luciferases; D051057:Proto-Oncogene Proteins c-akt; D007781:Lactoferrin