How cancer cells alter their metabolism and shape their distinctive metabolic milieu?, how cancer cells and other types of cell harness nutrients in their local environments (or Tumor MicroEnvironements, TMEs) for their benefits?, how systemic metabolism of the host affects TMEs and in turn influences the metabolism of cancer cells are major areas of focus in our lab.

The Lee lab conducts research that contributes to the treatment of cancer by understanding the altered metabolic behaviors of cancer cells and identifying vital metabolic mechanisms for cancer growth and survival.
The understanding of tumor metabolism has gained significant attention and has become the hallmark of cancer in recent decades. However, previous metabolic studies focused on cancer cells have had limitations due to the insufficient consideration of the tumor’s growing environment.

1. Our research team aims to analyze and elucidate the metabolic characteristics of the tumor microenvironment (TME) using cutting-edge technologies and ideas.
2. We observe how various types of cancer adapt to their unique metabolic environments through multi-omics approach and
3. further investigate key metabolic mechanisms required for tumor growth and survival in the context of in vivo using state-of-the-art genetically engineered mouse and surgical mouse models, and fresh tissue samples from cancer patients. Our research encompasses the development of therapies, starting from fundamental research to assess whether these key metabolic mechanisms can be utilized as treatment targets. The Lee lab eagerly awaits the support of motivated and curious students and researchers to work together in overcoming the unsolved challenges in the development of cancer treatments targeting metabolism.

Cancer Metabolism and Tumor MicroEnvironment
• ㆍDeciphering metabolic composition in Tumor MicroEnvironment (TME)
• ㆍCancer metabolism and behavior
• ㆍMetabolic competition/cooperation between Cancer cells and Other cell types
• ㆍSystemic metabolism and Cancer behavior
• ㆍMetabolic Tracing in Cell, Live animal, and Patient tissue

• ㆍM-S Lee, et al., (2023) Ornithine aminotransferase supports polyamine synthesis in pancreatic cancer. Nature 616(7956), 339-347
• ㆍP-Y Tsai and M-S Lee, et al., (2021) Adaptation of pancreatic cancer cells to nutrient deprivation is reversible and requires glutamine synthetase stabilization by mTORC1. PNAS 118(10), e2003014118
• ㆍM-S Lee and H-J Han, et al., (2018) Loss of the E3 ubiquitin ligase MKRN1 represses diet-induced metabolic syndrome through AMPK activation. Nature Communications 9(1), 3404
• ㆍH Xu and M-S Lee, et al., (2018) Ablation of insulin receptor substrates 1 and 2 suppresses Kras-driven lung tumorigenesis. PNAS 115 (16) 4228-4233
• ㆍM-S Lee, et al., (2015) PI3K/AKT activation induces PTEN ubiquitination and destabilization accelerating tumorigenesis. Nature Communications 6:7769
• ㆍM-S Lee, et al., (2013) Stabilization of p21 (Cip1/WAF1) following Tip60-dependent acetylation is required for p21-mediated DNA damage response. Cell death and differentiation 20, 620–629

• ㆍB.S., Sungkyunkwan University. Korea (2009)
• ㆍM.S., Sungkyunkwan University. Korea (2011)
• ㆍPh.D., Yonsei University. Korea (2016)

• ㆍ2016-2017 : Postdoctoral Fellow, Dept. of Biochemistry, Yonsei University, Korea
• ㆍ2017-2023 : Postdoctoral Fellow, Div. of Endocrinology, Boston Children’s Hospital/Harvard Medical School, USA
• ㆍ2023-Present : Assistant Professor, Dept. of Life Sciences, POSTECH, Korea