title: Regression of A549 lung cancer tumors by anti-miR-150 vector.
abstract: microRNAs (miRNAs) have been shown to play a role in cancer. Antisense oligonucleotides             can bind directly to miRNAs and block their activity, which are generally named             anti-miRNAs. To suppress A549 cell proliferation in vitro and in vivo by anti-miRNAs,             an anti-miR-150 expression vector (PR-ASO-150), regulated by the H1 promoter and             containing a 'TTTTT' sequence following a hairpin to stop transcription, was constructed.             A549 cell proliferation in vitro or in nude mice was observed after PR-ASO-150             treatment. Our results showed that miR-150 expression was inhibited and the growth             inhibition rate of A549 cells was higher in the PR-ASO-150-treated group compared             with the control, which indicated that PR-ASO-150 could inhibit A549 cell proliferation             by regulating miR-150 expression. Following establishment of A549 cancer cell             xenografts in nude mice, PR-ASO-150 was delivered intratumorally to investigate             the suppressive action to tumor proliferation by regulating miR-150 expression.             The results indicate that the tumor volume and weight were lower compared to the             control group. Our results further showed that p53 expression was higher after             tumor tissue was treated with PR-ASO-150, indicating that up-regulation of p53             contributed to the suppression to tumor growth. Our study provides a novel strategy             for cancer therapy through the development of anti-miRNAs.
authors.affiliation: Institute of Medical Molecular Genetics, Department of Biochemistry and Molecular Biology, Binzhou Medical University, Yan Tai 264003, PR China.
authors.forename: You-Jie
authors.initials: YJ
authors.lastname: Li
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Zhang
authors.forename: Ping-Yu
authors.initials: PY
authors.lastname: Wang
authors.forename: Yong-Liang
authors.initials: YL
authors.lastname: Chi
authors.forename: Chao
authors.initials: C
authors.lastname: Zhang
authors.forename: Ying
authors.initials: Y
authors.lastname: Ma
authors.forename: Chang-Jun
authors.initials: CJ
authors.lastname: Lv
authors.forename: Shu-Yang
authors.initials: SY
authors.lastname: Xie
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000235:genetics; D015153:Blotting, Western; D045744:Cell Line, Tumor; D005434:Flow Cytometry; D005822:Genetic Vectors / Q000235:genetics / Q000494:pharmacology*; D006801:Humans; D008175:Lung Neoplasms / Q000235:genetics*; D051379:Mice; D008819:Mice, Nude; D035683:MicroRNAs / Q000235:genetics*; D020320:Oligoribonucleotides, Antisense / Q000235:genetics / Q000494:pharmacology*; D011401:Promoter Regions, Genetic / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D014162:Transfection; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D023041:Xenograft Model Antitumor Assays
chemical_list: D000970:Antineoplastic Agents; D035683:MicroRNAs; D020320:Oligoribonucleotides, Antisense; D016159:Tumor Suppressor Protein p53; C533097:MIR150, human