Oncotarget

Reviews:

Multiple biological functions of Twist1 in various cancers

Zhixiang Zhao, Mohammad Aminur Rahman, Zhuo G. Chen and Dong M. Shin _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:20380-20393. https://doi.org/10.18632/oncotarget.14608

Metrics: PDF 3574 views  |   HTML 5132 views  |   ?  


Abstract

Zhixiang Zhao1,2,*, Mohammad Aminur Rahman1,*, Zhuo G. Chen1 and Dong M. Shin1

1 Department of Hematology and Medical Oncology, Winship Cancer Institute of Emory University, Atlanta, GA, United States of America

2 Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China

* These authors have contributed equally to this study

Correspondence to:

Dong M. Shin, email:

Keywords: twist1, EMT, stemness, angiogenesis, chemo-resistance

Received: June 29, 2016 Accepted: January 01, 2017 Published: January 12, 2017

Abstract

Twist1 is a well-known regulator of transcription during embryonic organogenesis in many species. In humans, Twist1 malfunction was first linked to Saethre-Chotzen syndrome and later identified to play an essential role in tumor initiation, stemness, angiogenesis, invasion, metastasis, and chemo-resistance in a variety of carcinomas, sarcomas, and hematological malignances. In this review, we will first focus on systematically elaborating the diverse pathological functions of Twist1 in various cancers, then delineating the intricate underlying network of molecular mechanisms, based on which we will summarize current therapeutic strategies in cancer treatment that target and modulate Twist1-involved signaling pathways. Most importantly, we will put special emphasis on revealing the independence and interdependency of these multiple biological functions of Twist1, piecing together the whole delicate picture of Twist1’s diversified pathological roles in different cancers and providing new perspectives to guide future research.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14608