Tan Suet Mien


Tan Suet Mien

Tan Suet Mien
Associate Professor


Office: 05n-08
Telephone: 6316 2834
Email: SMTan@ntu.edu.sg



  • BSc (1st Class Hons), MSc, National University of Singapore
  • D.Phil., Oxford University, UK

Professional Experience

  • Singapore Society for Biochemistry and Molecular Biology Medal, NUS, 1995
  • The Lijen Industrial Development Medal, NUS, 1995
  • Arthritis Research Campaign Scholarship, UK, 1998
  • Assistant Professor, School of Biological Sciences (SBS), NTU, 2001
  • Sub-Dean (Academic) 2005-2006
  • Assistant Chair (Academic) 2006-2008
  • Nanyang Award for Excellence in Teaching, NTU, 2006
  • Associate Chair (Academic), School of Biological Sciences, NTU, 1st July 2011 – 30th June 2014
  • National Day Honours (2013)
  • The Public Administration Medal (Bronze)

Research Interest

My research group has a long-standing interest in understanding the molecular mechanisms of cell adhesion and migration underpinning normal and pathological conditions, including inflammation and cancer. We focus on two families of molecules – integrins and kindlins. Integrins are heterodimeric transmembrane proteins that mediate cell-cell, cell-extracellular matrix, and cell-virus interactions. Integrin ligand-binding is regulated by its conformational change that is dependent on the interactions between its cytoplasmic domain and cytosolic proteins. These cytosolic proteins can either be positive or negative regulators of integrin function. Currently, my research group and in collaboration with others seek to define the molecular basis of cross-talks between these regulators, and how they modulate integrin ligand-binding, signaling and cytoskeletal re-modelling under normal and pathological conditions, such as chronic inflammation and cancer metastasis.

Kindlins are a small family of FERM-domain-containing cytoplasmic proteins. Three kindlin paralogs have been identified with dissimilar tissue expression profiles. Over the last few years, kindlins emerged as key regulators of integrin activation and signaling. The importance of kindlins is underscored by diseases Kindler syndrome, leukocyte adhesion deficiency III, and cancer. In addition to integrin-affinity regulation, our research group and others have shown that kindlins promote integrin clustering, which strengthens cell-ECM and cell-cell adhesion. There is also gaining evidence that kindlins are involved in cellular signaling conduits that are independent of integrins. We are investigating the roles of kindlins in these pathways in the context of cancer progression. Our recent work suggests an important role of kindlin3 in chronic myeloid leukemia cell proliferation. Some images for our research work and in collaboration with others are shown below.     

An illustration of intergrin signalling in antigen presentation 


Silencing of kindlin3 slows the growth of chronic myelogenous leukemia cells in soft agar and mouse xenograft.


Integrin LFA-1-mediated T cell migration on ICAM-1. Immunofluorescence imaging of cytosolic molecules RACK1 (A), kindlin3 (B), and MyH9 (C) (red). Actin (green) and nucleus (Blue). 

SEM images of melanoma cells with kindlin overexpression and mouse lung metastasis assay.

Wound healing assay to assess the effect of kindlin overexpression in cancer cells.

Analyses of force contractions of HUVECs on micro-posts coated with ECM. FN: fibronectin, COL: collagen

FRET analyses of integrin cytoplasmic tails interactions.    

Immunofluorescence analyses of HUVECs spreading on fibronectin. Stainings of kindlins, RACK1 and hnRNPK are shown.  

MD simulations of integrin transmembrane packing.