||Yinghui Li |
Nanyang Assistant Professor (NRF)
Telephone: 6316 2947
2013 Ph.D, Karolinska Institutet, Stockholm, Sweden (Medical Science)
2005 B.Sc. (Hons), National University of Singapore (Life Sciences)
2016 – 2017: Senior Research Fellow, Institute of Molecular and Cell Biology, Singapore
2013 – 2016: Research Fellow, Institute of Molecular and Cell Biology, Singapore
2007-2013: A*STAR Graduate Scholar (Overseas), Karolinska Institutet, Stockholm
2005-2006: Research Assistant, Department of Anatomy, National University of Singapore
My research interests focus on the molecular mechanisms underscoring the activation of cancer driver genes and the role of non-coding RNAs in the progression of human cancers. Recent advances in whole-genome sequencing have led to the identification of several somatic, non-coding mutations in a wide variety of human cancers. These mutations frequently occur in cis-regulatory regions i.e. non-coding, regulatory DNA including gene promoters, enhancers, silencers and insulators, which regulate the transcription of cancer-associated genes. Some of these mutations are recurrent in multiple cancer types and are associated with gene expression changes as well as clinical outcome of disease, thereby raising the possibility that they represent driver mutations in cancer. Besides cis-regulatory mutations, non-coding RNAs such as lncRNAs have been found to play significant roles in the transcriptional programs of cancer. One of their regulatory mechanisms involve the modulation of enhancer-promoter chromatin interactions to drive the expression of cancer driver genes during malignant development.
The main focus of my laboratory is to understand the role of inflammatory mediators such as NF-κB in activating transcriptional programs that are critical for the malignant transformation of cancer cells. We will use high-throughput methods such as ChIP sequencing and RNA sequencing that is complemented by genome-editing strategies as well as in vitro
and in vivo
functional assays, to uncover the underlying mechanisms and the impact of these factors in the transcriptional control of cancer development. These studies will lead to our eventual goal of identifying novel therapeutic targets and to develop new strategies for the selective disruption of cancer-specific transcriptional programs.