Taipei Medical University

Shu-Chun Chang

Shu-Chun Chang
https://hub.tmu.edu.tw/en/persons/shu-chun-chang

Research Field

Medicine

Introduction

Shu-Chun Chang is an Associate Professor of the Ph.D. Program for Translational Medicine, Taipei Medical University, Taiwan. Dr. Chang trained in extracellular biology and glycobiology and began work on cancer research as her PhD study in Imperial College London (IC, 2007-2011). Her PhD work aimed to investigate the role of Hedgehog Acyltransferase & Heparan Sulphate Proteoglycans (HSPGs) in Human Sonic Hedgehog (hShh) Signaling. These studies have greatly contributed to defining the functional roles of hShh interactions with HSPGs and palmitoylation of hShh in the formation of hShh multimeric complex, which enabled cancer cell therapeutics. Dr Chang continued to work in the field of Cancer Immunology/Inflammation as her Post-Doc research at the National University of Singapore (NUS, 2011-2015). Her findings clearly established the power of SAG-UPS (ubiquitin proteasome system) as a functional link between immune defense and apoptosis or immune-overactivation and tumorigenesis. SAG–UPS was proposed to be an efficient target for developing therapeutics against autoimmune diseases and cancers. Continuing from her postdoctoral research work, her current independent research focusses on: UPS, E2/E3 enzymes profiling, cancer therapeutics and anticancer strategies, the tumorigenic microenvironment, Hiltonol cocktails in anti-cancer strategies, anti-PD-L1 cancer vaccine. All of these related topics of research encompasses cancer immunomodulation, which she is being recognized internationally, as evidenced by multiple invitations from impactful journals to her to submit manuscripts to contribute her area of expertise.

Previously, Dr Chang revealed that dysregulation of the ubiquitination-proteasome system (UPS) exacerbates the tumor microenvironment and drives malignant transformation [1-3]. As the largest family of E3 ligases, the SCF E3 is involved in chronic inflammation-mediated tumorigenesis such as BRCA [4,5]. However, the underlying mechanisms and key factors through which SCF E3 ligase drives BRCA initiation and progression remain unclear. During Dr Chang's research period in TMU (2015-current), since her research encompasses a wide array of experimental approaches (e.g. biochemical, cell & molecular techniques, molecular biophysics, computational modeling and immunochemical methods involving clinical specimens), as a Principle Investigator, Dr Chang has put together a team of collaborators and co-workers (both locally at TMU and internationally) to derive the best output and to spawn research collegiality and inculcate team-spirit. In the future, Dr Chang aim to investigate  potent approaches to restrain the pro-tumorigenic microenvironment to inhibit cancer cell growth and metastasis.

 

References:

1. Chang, S.C.; Ding, J.L. Ubiquitination and SUMOylation in the chronic inflammatory tumor microenvironment. Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 2018, 1870, 165-175, doi:10.1016/j.bbcan.2018.08.002.
2. Chang, S.-C.; Yang, W.-C.V. Hyperglycemia, tumorigenesis, and chronic inflammation. Critical Reviews in Oncology/Hematology 2016, 108, 146-153, doi:10.1016/j.critrevonc.2016.11.003.
3. Chang, S.C.; Ding, J.L. SAG-UPS regulates malignant transformation--from chronic inflammation to pro-tumorigenesis to liver cancer. Cell Death Dis 2015, 6, e1941, doi:10.1038/cddis.2015.312.
4. Moris, D.; Kontos, M.; Spartalis, E.; Fentiman, I.S. The Role of NSAIDs in Breast Cancer Prevention and Relapse: Current Evidence and Future Perspectives. Breast Care (Basel) 2016, 11, 339-344, doi:10.1159/000452315.
5. Chang, S.C.; Ding, J.L. Ubiquitination by SAG regulates macrophage survival/death and immune response during infection. Cell Death & Differentiation 2014, 21, 1388-1398, doi:10.1038/cdd.2014.54.


Research Topics

A. BZDRs promote breast cancer progression through GABRA3-ECM signaling.

BZDRs (benzodiazepines and related Z-drugs) are widely prescribed for long-term use despite warnings of risk to physical and psychological tolerance and dependence. We and others have shown that BZDRs exacerbate breast cancer (BRCA) risk and metastasis. Although BZDRs are known to suppress neurotransmitters via GABA type A receptors, the mechanism underlying how BZDRs may promote cancer cell advancement is under-explored.  By retrospective analyses of clinical data, in silico predictions and further empirical tests, we highlight potential involvement of neuroinflammation pathway as a key signaling node in the crosstalk between GABRA3 and ECMs, which regulate signal transduction in the tumor microenvironment. In the future, it would be essential to investigate how BZDRs may effect tumor microenvironment (TME) in BRCA patients.

B. Clarify PBMCs-associated tumorigenic microenvironment mediated by Musa Sapientum extracts.

Non-small cell lung cancer (NSCLC), closely associated with chronic inflammation/immune overactivation, is a leading cause of cancer-related deaths in the world. Musa Sapientum extracts are reported to show potent anti-inflammatory activities via modulating cytokines production. However, whether and how Musa Sapientum extracts may mediate tumor microenvironment (TME) in NSCLC patients is still unknown. Previously, we showed that macrophages regulate ex-vivo cytokine production in response to different stimuli. We proposed that long-term inflammation/immune-overactivation conditions cause Mφ exacerbate the TME and drive malignant transformation. In current project, we hypothesize for the first time that Musa Sapientum extracts provide anti-cancer activities via suppressing TME in NSCLC patients. This work will have profound impact in development of anti-cancer therapies provided by Musa Sapientum extracts via modulating TME in NSCLC.


Honor

2023/10~present    Medical Consultant, Yu Chun Biotech CO., LTD, Taiwan 


Educational Background

2007~2011  Ph.D., Division of National Heart & Lung Institute, Faculty of Medicine, Imperial College London, UK
2011~2015  PostDoc Research Fellow, Department of Biological Sciences, National University of Singapore, Singapore