MicroRNA networks in pulmonary arterial hypertension: share mechanisms with cancer?

被引:23
作者
Courboulin, Audrey [1 ]
Ranchoux, Benoit [2 ]
Cohen-Kaminsky, Sylvia [1 ]
Perros, Frederic [1 ,2 ]
Bonnet, Sebastien [2 ]
机构
[1] Univ Paris 11, Univ Paris Saclay, Hop Marie Lannelongue, Fac Med,Inserm UMR S 999, Le Plessis Robinson, France
[2] Univ Quebec, Ctr Rech, Inst Univ Cardiol & Pneumol Quebec, Pulm Hypertens Res Grp, Quebec City, PQ, Canada
基金
加拿大健康研究院;
关键词
cancers; microRNA; pulmonary hypertension; SMOOTH-MUSCLE-CELLS; HEPATOCELLULAR-CARCINOMA CELL; TUMOR-SUPPRESSOR GENE; ACTIVATED T-CELLS; BREAST-CANCER; MESENCHYMAL TRANSITION; ESOPHAGEAL CANCER; MIR-17-92; CLUSTER; CHRONIC HYPOXIA; DOWN-REGULATION;
D O I
10.1097/CCO.0000000000000253
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Purpose of review Pulmonary arterial hypertension (PAH) is a rare disease with poor prognosis and no therapeutics. PAH is characterized by severe remodeling of precapillary pulmonary arteries, leading to increased vascular resistance, pulmonary hypertension compensatory right ventricular hypertrophy, then heart failure and death. PAH pathogenesis shares similarities with carcinogenesis such as excessive cell proliferation, apoptosis resistance, metabolic shifts, or phenotypic transition. Although PAH is not a cancer, comparison of analogous mechanisms between PAH and cancer led to the concept of a cancer-like disease to emerge. MicroRNAs (miRNAs) are small noncoding RNAs involved in the regulation of posttranscriptional gene expression. miRNA dysregulations have been reported as promoter of the development of various diseases including cancers. Recent findings Recent studies revealed that miRNA dysregulations also occur in PAH pathogenesis. In PAH, different miRNAs have been implicated to be the main features of PAH pathophysiology (in pulmonary inflammation, vascular remodeling, angiogenesis, and right heart hypertrophy). Summary The review summarizes the implication of miRNA dysregulation in PAH development and discusses the similarities and differences with those observed in cancers.
引用
收藏
页码:72 / 82
页数:11
相关论文
共 129 条
[1]   Silencing of stathmin induces tumor-suppressor function in breast cancer cell lines harboring mutant p53 [J].
Alli, E. ;
Yang, J-M ;
Hait, W. N. .
ONCOGENE, 2007, 26 (07) :1003-1012
[2]   Uncovering the clinical utility of miR-143, miR-145 and miR-224 for predicting the survival of bladder cancer patients following treatment [J].
Avgeris, Margaritis ;
Mavridis, Konstantinos ;
Tokas, Theodoros ;
Stravodimos, Konstantinos ;
Fragoulis, Emmanuel G. ;
Scorilas, Andreas .
CARCINOGENESIS, 2015, 36 (05) :528-537
[3]   NFκB-mediated cyclin D1 expression by microRNA-21 influences renal cancer cell proliferation [J].
Bera, Amit ;
Ghosh-Choudhury, Nandini ;
Dey, Nirmalya ;
Das, Falguni ;
Kasinath, Balakuntalam S. ;
Abboud, Hanna E. ;
Choudhury, Goutam Ghosh .
CELLULAR SIGNALLING, 2013, 25 (12) :2575-2586
[4]   Systems-level regulation of microRNA networks by miR-130/301 promotes pulmonary hypertension [J].
Bertero, Thomas ;
Lu, Yu ;
Annis, Sofia ;
Hale, Andrew ;
Bhat, Balkrishen ;
Saggar, Rajan ;
Saggar, Rajeev ;
Wallace, W. Dean ;
Ross, David J. ;
Vargas, Sara O. ;
Graham, Brian B. ;
Kumar, Rahul ;
Black, Stephen M. ;
Fratz, Sohrab ;
Fineman, Jeffrey R. ;
West, James D. ;
Haley, Kathleen J. ;
Waxman, Aaron B. ;
Chau, B. Nelson ;
Cottrill, Katherine A. ;
Chan, Stephen Y. .
JOURNAL OF CLINICAL INVESTIGATION, 2014, 124 (08) :3514-3528
[5]   Loss of miR-223 and JNK Signaling Contribute to Elevated Stathmin in Malignant Pleural Mesothelioma [J].
Birnie, Kimberly A. ;
Yip, Yan Y. ;
Ng, Dominic C. H. ;
Kirschner, Michaela B. ;
Reid, Glen ;
Prele, Cecilia M. ;
Musk, Arthur W. ;
Lee, Y. C. Gary ;
Thompson, Philip J. ;
Mutsaers, Steven E. ;
Badrian, Bahareh .
MOLECULAR CANCER RESEARCH, 2015, 13 (07) :1106-1118
[6]   Plexiform vasculopathy of severe pulmonary arterial hypertension and microRNA expression [J].
Bockmeyer, Clemens L. ;
Maegel, Lavinia ;
Janciauskiene, Sabina ;
Rische, Johanna ;
Lehmann, Ulrich ;
Maus, Ulrich A. ;
Nickel, Nils ;
Haverich, Axel. ;
Hoeper, Marius M. ;
Golpon, Heiko A. ;
Kreipe, Hans ;
Laenger, Florian ;
Jonigk, Danny .
JOURNAL OF HEART AND LUNG TRANSPLANTATION, 2012, 31 (07) :764-772
[7]   The nuclear factor of activated T cells in pulmonary arterial hypertension can be therapeutically targeted [J].
Bonnet, Sebastien ;
Rochefort, Gael ;
Sutendra, Gopinath ;
Archer, Stephen L. ;
Haromy, Alois ;
Webster, Linda ;
Hashimoto, Kyoko ;
Bonnet, Sandra N. ;
Michelakis, Evangelos D. .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (27) :11418-11423
[8]   Interleukin-6 Modulates the Expression of the Bone Morphogenic Protein Receptor Type II Through a Novel STAT3-microRNA Cluster 17/92 Pathway [J].
Brock, Matthias ;
Trenkmann, Michelle ;
Gay, Renate E. ;
Michel, Beat A. ;
Gay, Steffen ;
Fischler, Manuel ;
Ulrich, Silvia ;
Speich, Rudolf ;
Huber, Lars C. .
CIRCULATION RESEARCH, 2009, 104 (10) :1184-U139
[9]   Endothelin-1 in the lungs of patients with pulmonary hypertension [J].
Cacoub, P ;
Dorent, R ;
Nataf, P ;
Carayon, A ;
Riquet, M ;
Noe, E ;
Piette, JC ;
Godeau, P ;
Gandjbakhch, I .
CARDIOVASCULAR RESEARCH, 1997, 33 (01) :196-200
[10]   A Role for miR-145 in Pulmonary Arterial Hypertension Evidence From Mouse Models and Patient Samples [J].
Caruso, Paola ;
Dempsie, Yvonne ;
Stevens, Hannah C. ;
McDonald, Robert A. ;
Long, Lu ;
Lu, Ruifang ;
White, Kevin ;
Mair, Kirsty M. ;
McClure, John D. ;
Southwood, Mark ;
Upton, Paul ;
Xin, Mei ;
van Rooij, Eva ;
Olson, Eric N. ;
Morrell, Nicholas W. ;
MacLean, Margaret R. ;
Baker, Andrew H. .
CIRCULATION RESEARCH, 2012, 111 (03) :290-300