![]() Our research may provide valuable insights into the mechanisms underlying human embryonic development and developmental disorders. Recently, we found that Tfcp2l1-mediated fatty acid oxidation plays a critical role in maintaining ESC survival during metabolic stress (Yan et al., EMBO Reports, 2021). Currently, we are studying the metabolic stress responses of ESCs. Our research has shown that p53 plays an essential role in regulating ESC differentiation after DNA damage by down-regulating the transcription of many ES cell critical genes (Li et al., Cell Stem Cell, 2015 Zhang et al., Cell Cycle, 2013 Li et al., Molecular Cell, 2012 Lee et al., PNAS, 2010). To address this question, we have studied how the tumor suppressor protein p53 regulates the DNA damage responses of ESCs. Despite this importance, the mechanisms by which ESCs maintain genome stability in response to DNA damage insults are poorly understood. As ESCs have the potential to differentiate into many different cell types and are a promising source for cell therapy, maintaining genomic stability and homeostasis is crucial for proper lineage choice. Interest 1: Transcriptional and epigenetic stress responses of embryonic stem cells. By conducting basic research on these transcription factors, we aim to generate novel insights into tumorigenesis and develop new methods of eliminating cancer cells. With extensive experience in embryonic stem cells (ESCs), mesenchymal stromal/stem cells (MSCs), and osteosarcoma (OS), we collaborate with intramural and extramural colleagues to study breast cancer. However, we have recently expanded our research to include transcription factors (e.g., RUNXs, CBFB) that interact with p53. To date, we have primarily focused on studying the tumor suppressor p53, also known as the guardian of the genome. Specifically, my laboratory investigates the biological functions of transcription factors that play critical roles in both stem cell and cancer biology. ![]() My research interest centers around understanding gene expression regulation in both stem cells and cancer cells.
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