Date: 20 January 2026 (Tuesday)
Time: 12:00 pm – 1:00 pm
Venue: Lecture Theatre 1, G/F, William M.W. Mong Block, 21 Sassoon Road 
Host: Professor Jason Wong

Dr Yinghui Li is a Nanyang Assistant Professor in the School of Biological Sciences, Nanyang Technological University Singapore and an EMBO Global Investigator. Dr Li leads a multi-disciplinary research program in cancer epigenomics, cell signalling, and RNA biology. Her lab’s research is focused on understanding how inflammation-driven signalling shapes transcriptional programs and chromatin function in cancer. In her early career, Dr Li discovered that de novo NF-κB sites were generated in the TERT promoter, linking inflammation to the increased survival of transformed cells. Following this, recent studies by her group have uncovered the mechanisms through which the TWEAK/Fn14 and non-canonical NF-κB pathways alter the cancer cell epigenome and transcriptome to drive cancer progression.

Inflammation-driven signalling networks reprogram the epigenome and transcriptional states of cancer and various diseases. Among these pathways, tumour necrosis factor receptor (TNFR) signalling—particularly the TWEAK/Fn14 axis and NF-κB pathway—emerge as potent drivers of tumour aggressiveness, therapeutic resistance, metabolic dysfunction, and metastasis. Yet, the molecular effectors that translate TNFR signalling into disease-specific gene expression programs remain poorly understood. Increasing evidence suggests that long non-coding RNAs (lncRNAs) and their associated RNA-binding proteins, as well as epigenome reprogramming play critical roles in shaping these pathogenic transcriptional states. We have identified an oncogenic lncRNA, PLUM, which is activated by NF-κB through the epigenome and mediates chemoresistance in multiple myeloma by interacting with EZH2, the catalytic subunit of Polycomb Repressive Complex 2. Interestingly, a distinct malignant plasma cell population displaying elevated PLUM-regulated gene signature is observed in relapsed multiple myeloma patients. These plasma cells display enhanced oxidative phosphorylation, metabolic and stress-adaptation programs, along with the suppression of interferon and inflammatory responses. Our findings support a model in which PLUM-associated programs contribute to a sustained, therapy-resistant malignant cell state. Hence, targeting PLUM-EZH2 interactions may represent a clinically potent strategy for the treatment of relapsed, refractory cancers harbouring aberrant EZH2 activity.