YAP and TAZ in Lung Cancer: Oncogenic Role and Clinical Targeting

被引:98
作者
Lo Sardo, Federica [1 ]
Strano, Sabrina [2 ]
Blandino, Giovanni [1 ]
机构
[1] Regina Elena Inst Canc Res, Oncogen & Epigenet Unit, Mol Med Area, Via Elio Chianesi 53, I-00144 Rome, Italy
[2] Regina Elena Inst Canc Res, Mol Chemoprevent Grp, Mol Med Area, Via Elio Chianesi 53, I-00144 Rome, Italy
关键词
YAP/TAZ; lung cancer; NSCLC; therapeutic targets; YES-ASSOCIATED PROTEIN; GROWTH-FACTOR RECEPTOR; POTENTIAL THERAPEUTIC TARGET; TYROSINE KINASE INHIBITORS; SQUAMOUS-CELL CARCINOMA; SERUM P53 ANTIBODIES; HIPPO PATHWAY; TUMOR-SUPPRESSOR; DOWN-REGULATION; BREAST-CANCER;
D O I
10.3390/cancers10050137
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Lung cancer is the leading cause of cancer death in the world and there is no current treatment able to efficiently treat the disease as the tumor is often diagnosed at an advanced stage. Moreover, cancer cells are often resistant or acquire resistance to the treatment. Further knowledge of the mechanisms driving lung tumorigenesis, aggressiveness, metastasization, and resistance to treatments could provide new tools for detecting the disease at an earlier stage and for a better response to therapy. In this scenario, Yes Associated Protein (YAP) and Trascriptional Coactivator with PDZ-binding motif (TAZ), the final effectors of the Hippo signaling transduction pathway, are emerging as promising therapeutic targets. Here, we will discuss the most recent advances made in YAP and TAZ biology in lung cancer and, more importantly, on the newly discovered mechanisms of YAP and TAZ inhibition in lung cancer as well as their clinical implications.
引用
收藏
页数:29
相关论文
共 239 条
[1]   Implications of MDSCs-targeting in lung cancer chemo-immunotherapeutics [J].
Adah, Dickson ;
Hussain, Muzammal ;
Qin, Limei ;
Qin, Li ;
Zhang, Jiancun ;
Chen, Xiaoping .
PHARMACOLOGICAL RESEARCH, 2016, 110 :25-34
[2]   Methylation associated inactivation of RASSF1A from region 3p21.3 in lung, breast and ovarian tumours [J].
Agathanggelou, A ;
Honorio, S ;
Macartney, DP ;
Martinez, A ;
Dallol, A ;
Radar, J ;
Fullwood, P ;
Chauhan, A ;
Walker, R ;
Shaw, JA ;
Hosoe, S ;
Lerman, MI ;
Minna, JD ;
Maher, ER ;
Latif, F .
ONCOGENE, 2001, 20 (12) :1509-1518
[3]   The Hippo pathway, p53 and cholesterol [J].
Aylon, Yael ;
Oren, Moshe .
CELL CYCLE, 2016, 15 (17) :2248-2255
[4]   YAP/TAZ Incorporation in the β-Catenin Destruction Complex Orchestrates the Wnt Response [J].
Azzolin, Luca ;
Panciera, Tito ;
Soligo, Sandra ;
Enzo, Elena ;
Bicciato, Silvio ;
Dupont, Sirio ;
Bresolin, Silvia ;
Frasson, Chiara ;
Basso, Giuseppe ;
Guzzardo, Vincenza ;
Fassina, Ambrogio ;
Cordenonsi, Michelangelo ;
Piccolo, Stefano .
CELL, 2014, 158 (01) :157-170
[5]   Clinician Roles in Early Integrated Palliative Care for Patients with Advanced Cancer: A Qualitative Study [J].
Back, Anthony L. ;
Park, Elyse R. ;
Greer, Joseph A. ;
Jackson, Vicki A. ;
Jacobsen, Juliet C. ;
Gallagher, Emily R. ;
Temel, Jennifer S. .
JOURNAL OF PALLIATIVE MEDICINE, 2014, 17 (11) :1244-1248
[6]   The Hippo superhighway: signaling crossroads converging on the Hippo/Yap pathway in stem cells and development [J].
Barry, Evan R. ;
Camargo, Fernando D. .
CURRENT OPINION IN CELL BIOLOGY, 2013, 25 (02) :247-253
[7]   TAZ is required for metastatic activity and chemoresistance of breast cancer stem cells [J].
Bartucci, M. ;
Dattilo, R. ;
Moriconi, C. ;
Pagliuca, A. ;
Mottolese, M. ;
Federici, G. ;
Di Benedetto, A. ;
Todaro, M. ;
Stassi, G. ;
Sperati, F. ;
Amabile, M. I. ;
Pilozzi, E. ;
Patrizii, M. ;
Biffoni, M. ;
Maugeri-Sacca, M. ;
Piccolo, S. ;
De Maria, R. .
ONCOGENE, 2015, 34 (06) :681-690
[8]   Akt phosphorylates the Yes-associated protein, YAP, to induce interaction with 14-3-3 and attenuation of p73-mediated apoptosis [J].
Basu, S ;
Totty, NF ;
Irwin, MS ;
Sudol, M ;
Downward, J .
MOLECULAR CELL, 2003, 11 (01) :11-23
[9]  
Begnaud Abbie, 2016, Am Soc Clin Oncol Educ Book, V35, pe468, DOI 10.14694/EDBK_159195
[10]   Lipid metabolic reprogramming in cancer cells [J].
Beloribi-Djefaflia, S. ;
Vasseur, S. ;
Guillaumond, F. .
ONCOGENESIS, 2016, 5 :e189-e189