Abstract
MicroRNAs (miRNAs) have recently emerged as an important new class of cellular regulators that control various cellular processes and are implicated in human diseases, including cancer. Here, we show that loss of let-7 function enhances lung tumor formation in vivo, strongly supporting the hypothesis that let-7 is a tumor suppressor. Moreover, we report that exogenous delivery of let-7 to established tumors in mouse models of non-small-cell lung cancer (NSCLC) significantly reduces the tumor burden. These results demonstrate the therapeutic potential of let-7 in NSCLC and point to miRNA replacement therapy as a promising approach in cancer treatment.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Base Sequence
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Carcinoma, Non-Small-Cell Lung / genetics*
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Carcinoma, Non-Small-Cell Lung / pathology
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Carcinoma, Non-Small-Cell Lung / therapy
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Cell Line, Tumor
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Humans
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Lung / metabolism
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Lung / pathology
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Lung Neoplasms / genetics*
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Lung Neoplasms / pathology
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Lung Neoplasms / therapy
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Mice
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Mice, Inbred NOD
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Mice, SCID
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MicroRNAs / administration & dosage
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MicroRNAs / genetics*
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RNA, Antisense / administration & dosage
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RNA, Antisense / genetics
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Reverse Transcriptase Polymerase Chain Reaction
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Tumor Burden
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Xenograft Model Antitumor Assays*
Substances
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MicroRNAs
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RNA, Antisense
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mirnlet7 microRNA, human