Academic Profile

Academic Qualifications
1994-1997 Doctor of Philosophy, National University of Singapore
1992-1993 Bachelor of Science (Hons), National University of Singapore
1989-1991 Bachelor of Science, National University of Singapore

Professional Experience
2019-present Associate Professor (tenured), LKCmedicine (70%), School of
Biological Sciences (30%), NTU
2016-2018 Associate Professor (tenured), LKCmedicine (30%)
2014-2018 Associate Chair (Student), School of Biological Sciences, NTU
2014-2018 Associate Professor (tenured), School of Biological Sciences,
NTU (70%)
2014 The Commendation Medal (Prime Minister’s Office)
2013 Nanyang Education Award (College)
2012 Nanyang Award for Research Excellence
2011 College of Science Collaborative Research Award
2007 Nanyang Education Award (School)

2016-present Board member, Skin Research Society (Singapore)
2014-present Active member, American Association for Cancer Research
2014-present Active member, American Society of Gene & Cell Therapy.
2013-present Fellows of the Teaching Excellence Academy, NTU
Andrew-1.jpg picture
Assoc Prof Tan Nguan Soon
Associate Professor, Metabolic Disorders and Vice Dean (Faculty Affairs)
Associate Professor, Lee Kong Chian School of Medicine
Associate Professor of Metabolic Disorders, School of Biological Sciences (SBS)

Metastasis accounts for more than 90% of cancer mortality. Once metastasis occurs, surgical excision of the primary tumor no longer guarantees disease free survival and the probability of cancer relapse in distal organs increases significantly. Although most cancer deaths are the result of metastases, cancer research has mainly focused on the primary tumor. Our findings have established several paradigms in oxidative stress-driven metastasis. Tumor cells become migratory and invasive via epithelial-mesenchymal transition (EMT). My lab has actively interrogated the molecular and metabolic changes in cancer cells during EMT. We showed that EMT is an energy-demanding process and that metabolic changes during EMT are critical to sustain an elevated adenylate energy charge needed to fuel various biological processes, such as invasion and chemoresistance. Our current interest aims to decipher the mechanisms that regulate and coordinate the different networks during EMT which will provide much-needed insight into the process of metastasis. Deliberate disruption of these mechanisms is expected to yield important clinical information regarding etiology, prognosis and response to therapy.

METABOLIC DISEASES (Nonalcoholic fatty liver disease, NAFLD)
NAFLD includes a spectrum of liver diseases that begin with lipid accumulation in the liver, also known as simple steatosis or NAFL. Over time, NAFL may gradually progress to the development of chronic inflammation (e.g., nonalcoholic steatohepatitis, or NASH), fibrosis and, ultimately, cirrhosis. NAFLD is an impending epidemic that affects 25% of the population worldwide. It is quickly becoming the leading cause of liver disease worldwide and has an increased prevalence of 40% in multiple westernized Asian countries (including Singapore). There is no FDA-approved treatment for NASH, and liver transplantation is the only proven treatment for end-stage liver disease. Recent FDA guidelines have highlighted the use of relevant animal models for the development of investigational drugs/therapies against noncirrhotic NASH with liver fibrosis. We have developed a novel NASH model that recapitulates the various transitory stages of human NAFLD and comorbidities such as insulin resistance and obesity. This NASH model is an efficient preclinical model for the validation of pharmacological candidates and nutritional interventions. We investigates the intimate relationship between gut microbes and the liver, the latter of which exploits prebiotics to rehabilitate gut microbes and microbial-derived metabolites to modify translatable mechanisms that affect hepatic metabolic flux and inflammation.

Poor healing wounds represent a silent epidemic that affects a large fraction of the world population and carries a heavy socioeconomic burden. Despite the enormous impact of these poor-healing wounds, effective therapies remain lacking. Effective management of these problems will require better understanding of the healing process to allow the creation of a salubrious environment conducive to healing. Our lab has worked extensively to understand the transcriptional regulation of skin wound healing and particularly the interplay among different cell types during wound healing. We identified angiopoietin-like 4 protein (ANGPTL4) as a novel matricellular protein that is essential for proper wound healing. Wound healing in ANGPTL4-knockout mice are delayed and share many characteristics of poor healing wounds, including increased/prolonged inflammation, impaired wound-related angiogenesis and ruined extracellular matrix. Thus, our current studies is to investigate the role of immune-associated reactive oxygen species on wound healing.
  • Bedside to bench and back again: evaluating Neisseria novel respiratory pathobionts using systems biology

  • Bioactive Stem Cells Secretome-Enriched Hydrogels For Chronic Wound Healing

  • Portable SERS-based Breathalyzer for Rapid and Online COVID-19 Detection and Surveillance

  • Portable SERS-based Breathalyzer for Rapid and Online COVID-19 Detection and Surveillance (Phase 2)

  • Relaxin treatment of liver fibrosis and vascular dysfunction using a novel animal model of non-alchoholic steatohepatits

  • Role of angiopoietin-like 4 in nonalcoholic steatohepatitis progression.

  • Targeting Brain Tumors: Improving Lives Through Precision Medicine
  • Cheng, H.S., Marvalim, C., Zhu, P.C., Law, C.L.D., Low, Z.Y.J., Chong, Y.K., Ang, B.T., Tang, C. and Tan, N.S. (2021) Kinomic profile in patient-derived glioma-propagating cells during hypoxia reveals c-MET-PI3K dependency for adaptation. Theranostics 11(11):5127-5142

  • Shin, E.M., Huynh, V.T., Neja, S.A., Liu, C.Y., Raju, A., Tan, K., Tan, N.S., Gunaratne, J., Bi, X., Iyer, L.M., Aravind, L., and Tergaonkar, V. GREB1: an evolutionarily conserved inducible mammalian cytoplasmic O-GlcNAc glycosyltransferase links hormone receptor stability to cancer. Science Advances 7(12):eabe2470

  • Suzuki, T., Ishii, S., Shinohara, M., Kawano, Y., Wakahashi, K., Kawano, H., Sada, A., Minagawa, K., Hamada, M., Takahashi, S., Furuyashiki, T., Tan, N.S., Matsui, T., Katayama, Y. (2020). Mobilization efficiency is critically regulated by fat via marrow PPARδ in mice. Haematologica. (in press)

  • Tan, M.W.I., Tan, W.R., Kong, Z.Q., Toh, J.H., Wee, W.K.J., Teo, E.M.L., Cheng, H.S., Wang, X.M. and Tan, N.S. (2020). High glucose restrains acetylcholine-induced keratinocyte EMT is mitigated by p38 inhibition. J. Invest. Dermatol. DOI: 10.1016/j.jid.2020.10.026

  • Zhang, Y., Liu, M., Peng, B., Jia, S., Koh, D., Wang, Y., Cheng, H.S., Tan, N.S., Warth, B., Chen, D., Fang, ML. (2020) Impact of Mixture Effects between Emerging Organic Contaminants on Cytotoxicity: A Systems-Biological Understanding of Synergism between TDCPP and TPP. Environ. Sci. Technol. Sep 1;54(17):10722-10734. doi: 10.1021/acs.est.0c02188

  • Wu, Z., Lim, H.K., Tan, S.J., Gautum, A., Hou, H.W., Ng, K.W., Tan, N.S. and Tay, C.Y. (2020) Potent-by-design: amino acids mimicking porous nanotherapeutics with intrinsic anti-cancer targeting properties. Small Aug;16(34):e2003757. doi: 10.1002/smll.202003757.

  • Jung, K.H., Sonm M.K., Yan, H.H., Fang, Z., Kim, J.Y., Kim, S.J., Park, J.H., Lee, J.E., Yoon, Y-C., Seo, M.S., Han, B.S., Ko, S., Lim, J.H., Lee, D-H., Teo, Z., Wee, W.K.J., Tan, N.S.* and Hong, S-S.* (2020) ANGPTL4 exacerbates pancreatitis by augmenting acinar cell injury through upregulation of C5a. EMBO Mol. Med. Aug 7;12(8):e11222. doi: 10.15252/emmm.201911222. co-corresponding

  • Kao, Y-C., Han, X., Lee, Y.H., Lee, H.K., Phan, G.C., Lay, C.L., Sim, H.Y.F., Ku, C.W., Tan, T.C., Tan, N.S.* and Li, X.Y.* (2020). SERS-based Metabolomics for Rapid and Non-invasive Diagnosis of Spontaneous Miscarriage. ACS Nano (DOI: 10.1021/acsnano.0c00515) *co-corresponding

  • Li, L., Foo, B., Kwok, K.W., Sakamoto, N., Mukae, H., Izumikawa, H., Mandard, S., Quenot, J-P., Lagrost, L., Teh, W.K., Kohli, G.S., Zhu, P.C., Choi, H., Buist, M., Seet, J.E., Yang, L., He, F., Chow, V. and Tan, N.S. (2019) Antibody treatment against angiopoietin-like 4 reduces pulmonary edema and injury in secondary pneumococcal pneumonia. mBio 10:e02469-18.

  • Cheng, H.S., Lee, J.X.T., Wahli, W. and Tan, N.S. (2019) Exploiting vulnerabilities of cancer by targeting nuclear receptors of stromal cells in tumor microenvironment. Mol. Cancer Mar 30;18(1):51. doi: 10.1186/s12943-019-0971-9.

  • Liao, Z., Chua, D. and Tan, N.S. (2019) Reactive oxygen species: a volatile driver of field cancerization and metastasis. Mol. Cancer Mar 30;18(1):65. doi: 10.1186/s12943-019-0961-y

  • Lim, M.M.K., Wee, J.W.K.,Soong, J.C., Chua, D., Tan, W.R., Lizwan, M., Li, Y., Teo, Z., Goh, W.W.B., Zhu, P.C. and Tan, N.S. (2018) Targeting metabolic flexibility via angiopoietin-like 4 protein sensitizes metastatic cancer cells to chemotherapy drugs. Mol. Cancer 17(1):152. doi: 10.1186/s12943-018-0904-z.

  • Lim, H.Y., Lim S.Y., Tan, C.K., Goh, C.C., See, P., Chakarov, S., Carbajo, D., Wang, X.N., Lim, L.H., Thiam, C.H., Johnson, L.A., Basu, R., Yeo, K.P., Chew, S.H.S., Goh, C., Evrard, M., Wang, J.K., Tan, Y., Jain, R., Tikoo, S., Jackson, D.G., Choong, C., Weninger, W., Poidinger, M., Stanley, R.E., Collin, M., Tan, N.S., Ng, L.G., Ginhoux, F. and Angeli, V. (2018). Hyaluronan receptor LYVE-1 expressing macrophages maintain arterial tone through hyaluronan-mediated regulation of smooth muscle cell collagen. Immunity. 49(2):326-341.e7. doi: 10.1016/j.immuni.2018.06.008.

  • Tan, E.H.P., Sng, M.K., How, I.S.B., Chan, J.S.K., Chen, J., Tan, C.K., Wahli, W. and Tan, N.S. (2018) ROS release by PPAR/δ-null fibroblasts reduces tumor load through epithelial antioxidant response. Oncogene doi:10.1038/s41388-017-0109-8

  • Chan, J.S.K., Sng, M.K., Teo, Z.Q., Chong, H.C., Twang, J.S. and Tan, N.S. (2018) Targeting nuclear receptors in cancer-associated fibroblasts as concurrent therapy to inhibit development of chemoresistant tumors. Oncogene 37(2):160-173. doi: 10.1038/onc.2017.319