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Articles by C Taccioli
Total Records ( 2 ) for C Taccioli
  S Volinia , M Galasso , S Costinean , L Tagliavini , G Gamberoni , A Drusco , J Marchesini , N Mascellani , M. E Sana , R Abu Jarour , C Desponts , M Teitell , R Baffa , R Aqeilan , M. V Iorio , C Taccioli , R Garzon , G Di Leva , M Fabbri , M Catozzi , M Previati , S Ambs , T Palumbo , M Garofalo , A Veronese , A Bottoni , P Gasparini , C. C Harris , R Visone , Y Pekarsky , A de la Chapelle , M Bloomston , M Dillhoff , L. Z Rassenti , T. J Kipps , K Huebner , F Pichiorri , D Lenze , S Cairo , M. A Buendia , P Pineau , A Dejean , N Zanesi , S Rossi , G. A Calin , C. G Liu , J Palatini , M Negrini , A Vecchione , A Rosenberg and C. M. Croce
 

We studied miRNA profiles in 4419 human samples (3312 neoplastic, 1107 nonmalignant), corresponding to 50 normal tissues and 51 cancer types. The complexity of our database enabled us to perform a detailed analysis of microRNA (miRNA) activities. We inferred genetic networks from miRNA expression in normal tissues and cancer. We also built, for the first time, specialized miRNA networks for solid tumors and leukemias. Nonmalignant tissues and cancer networks displayed a change in hubs, the most connected miRNAs. hsa-miR-103/106 were downgraded in cancer, whereas hsa-miR-30 became most prominent. Cancer networks appeared as built from disjointed subnetworks, as opposed to normal tissues. A comparison of these nets allowed us to identify key miRNA cliques in cancer. We also investigated miRNA copy number alterations in 744 cancer samples, at a resolution of 150 kb. Members of miRNA families should be similarly deleted or amplified, since they repress the same cellular targets and are thus expected to have similar impacts on oncogenesis. We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted. Other miRNAs, such as hsa-miR-30 and hsa-miR-204, were found to be physically altered at the DNA copy number level as well. By combining differential expression, genetic networks, and DNA copy number alterations, we confirmed, or discovered, miRNAs with comprehensive roles in cancer. Finally, we experimentally validated the miRNA network with acute lymphocytic leukemia originated in Mir155 transgenic mice. Most of miRNAs deregulated in these transgenic mice were located close to hsa-miR-155 in the cancer network.

  G Di Leva , P Gasparini , C Piovan , A Ngankeu , M Garofalo , C Taccioli , M. V Iorio , M Li , S Volinia , H Alder , T Nakamura , G Nuovo , Y Liu , K. P Nephew and C. M. Croce
  Background

Several lines of evidence have suggested that estrogen receptor (ER)–negative breast tumors, which are highly aggressive and nonresponsive to hormonal therapy, arise from ER-positive precursors through different molecular pathways. Because microRNAs (miRNAs) modulate gene expression, we hypothesized that they may have a role in ER-negative tumor formation.

Methods

Gene expression profiles were used to highlight the global changes induced by miRNA modulation of ER protein. miRNA transfection and luciferase assays enabled us to identify new targets of miRNA 206 (miR-206) and miRNA cluster 221-222 (miR-221-222). Northern blot, luciferase assays, estradiol treatment, and chromatin immunoprecipitation were performed to identify the miR-221-222 transcription unit and the mechanism implicated in its regulation.

Results

Different global changes in gene expression were induced by overexpression of miR-221-222 and miR-206 in ER-positive cells. miR-221 and -222 increased proliferation of ER-positive cells, whereas miR-206 had an inhibitory effect (mean absorbance units [AU]: miR-206: 500 AU, 95% confidence interval [CI]) = 480 to 520; miR-221: 850 AU, 95% CI = 810 to 873; miR-222: 879 AU, 95% CI = 850 to 893; P < .05). We identified hepatocyte growth factor receptor and forkhead box O3 as new targets of miR-206 and miR-221-222, respectively. We demonstrated that ER negatively modulates miR-221 and -222 through the recruitment of transcriptional corepressor partners: nuclear receptor corepressor and silencing mediator of retinoic acid and thyroid hormone receptor.

Conclusions

These findings suggest that the negative regulatory loop involving miR-221-222 and ER may confer proliferative advantage and migratory activity to breast cancer cells and promote the transition from ER-positive to ER-negative tumors.

 
 
 
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