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Author Notes:
Correspondence to: Dong M. Shin, email: dmshin@emory.edu
We owe special thanks to Dr. Anthea Hammond for her critical comments and editorial review of this article.
No potential conflicts of interest were disclosed.
Subjects:
Research Funding:
This work was supported by grants from the NCI of the NIH under award number U01CA151802.
Keywords:
- Science & Technology
- Life Sciences & Biomedicine
- Oncology
- Cell Biology
- twist1
- EMT
- stemness
- angiogenesis
- chemo-resistance
- EPITHELIAL-MESENCHYMAL TRANSITION
- SQUAMOUS-CELL CARCINOMA
- SAETHRE-CHOTZEN-SYNDROME
- TRANSCRIPTION FACTORS SNAIL
- CADHERIN GENE-EXPRESSION
- BREAST-CANCER
- HEPATOCELLULAR-CARCINOMA
- UP-REGULATION
- NASOPHARYNGEAL CARCINOMA
- BLADDER-CANCER
Multiple biological functions of Twist1 in various cancers
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.
Copyright information:
© 2017 Zhao et al.
This is an Open Access work distributed under the terms of the Creative Commons Attribution 3.0 Unported License (http://creativecommons.org/licenses/by/3.0/).
