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  • BREAST-CANCER METASTASIS  (1)
  • Breast Neoplasms/*drug therapy/*pathology  (1)
  • 1
    Keywords: GROWTH ; LUNG-CANCER ; NF-KAPPA-B ; TRANSCRIPTION FACTOR ; mechanisms ; DUCTAL ADENOCARCINOMA ; TUMOR LYMPHANGIOGENESIS ; BREAST-CANCER METASTASIS ; HUMAN-ENDOTHELIAL-CELLS ; PROMOTES ANGIOGENESIS
    Abstract: Recent advances in cancer biology have emerged important roles for microRNAs (miRNAs) in regulating tumor responses. However, their function in mediating intercellular communication within the tumor microenvironment is thus far poorly explored. Here, we found miR-206 to be abrogated in human pancreatic ductal adenocarcinoma (PDAC) specimens and cell lines. We show that miR-206 directly targets the oncogenes KRAS and annexin a2 (ANXA2), thereby acting as tumor suppressor in PDAC cells by blocking cell cycle progression, cell proliferation, migration and invasion. Importantly, we identified miR-206 as a negative regulator of oncogenic KRAS-induced nuclear factor-kappa B transcriptional activity, resulting in a concomitant reduction of the expression and secretion of pro-angiogenic and pro-inflammatory factors including the cytokine interleukin-8, the chemokines (C-X-C motif) ligand 1 and (C-C motif) ligand 2, and the granulocyte macrophage colony-stimulating factor. We further show that miR-206 abrogates the expression and secretion of the potent pro-lymphangiogenic factor vascular endothelial growth factor C in pancreatic cancer cells through an NF-kappa B-independent mechanism. By using in vitro and in vivo approaches, we reveal that re-expression of miR-206 in PDAC cells is sufficient to inhibit tumor blood and lymphatic vessel formation, thus leading to a significant delay of tumor growth and progression. Taken together, our study sheds light onto the role of miR-206 as a pleiotropic modulator of different hallmarks of cancer, and as such raising the intriguing possibility that miR-206 may be an attractive candidate for miRNA-based anticancer therapies.
    Type of Publication: Journal article published
    PubMed ID: 25500542
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  • 2
    Publication Date: 2014-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Keklikoglou, Ioanna -- De Palma, Michele -- England -- Nature. 2014 Nov 6;515(7525):46-7. doi: 10.1038/nature13931. Epub 2014 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Swiss Institute for Experimental Cancer Research, School of Life Sciences, Ecole Polytechnique Federale de Lausanne (EPFL), 1015 Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25337881" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*drug therapy/*pathology ; Chemokine CCL2/*antagonists & inhibitors/*metabolism ; Female ; *Neoplasm Metastasis ; *Neovascularization, Pathologic
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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