Our research focus

Apoptosis

Cellular fate is controlled by multiple molecular pathways. The most studied is apoptosis, a form of programmed cell death used by all multicellular organisms to eliminate cells which are damaged, no longer needed or which might become a threat to the organism. This process is often deregulated in cancer cells allowing them to survive and proliferate when otherwise they should be eliminated.

BH3 mimetics

Dysfunctional apoptosis can cause or accelerate cancer development, but also underlies resistance to common cancer treatment approaches such as chemotherapy. Members of a particular family of proteins (the “BCL-2” proteins) are critical regulators of apoptosis. Recently, a new class of drugs called “BH3 mimetics” have been developed to target some BCL-2 proteins and activate apoptosis, leading to tumour cell death. One of these drugs is now being used in the clinic to treat some blood cancers, and others are under extensive investigation, including by our lab.

Autophagy

Autophagy is predominantly a process that enables cells to survive under stressful conditions such as when nutrients are in short supply. Like apoptosis, it can also become dysfunctional in cancer. Under some circumstance, proteins that regulate autophagy can also interact with those involved in apoptosis. This is a particular interest of our lab as it might have important implications for how cancer cell survive abnormally.

Fast facts

This term encompasses events such as when a cell receives external cues (e.g. from factors like proteins in the blood) and transmits them inside the cell to activate processes such as cell division, movement and death. Cells can also signal to other cells by secreting molecules such as proteins.

Under normal conditions,  apoptosis is essential to remove old, damaged or dangerous cells. In cancer, this process is often switched off allowing abnormal cells to survive and grow when they should otherwise be killed and eliminated.

Primarily, a cell survival process meaning to “self eat”. In times of stress, nutrient deprivation or infection, the cell eats its own components in order to maintain cellular energy levels, or to remove unwanted materials (such as viruses and non-functioning protein aggregates) allowing it to survive.

Recent publications

Nature

BCL-XL and MCL-1 Are the Key BCL-2 Family Proteins in Melanoma Cell Survival

DOI: 10.1038/s41419-019-1568-3

View abstract
Autophagy

Structural Insights Into BCL2 Pro-Survival Protein Interactions With the Key Autophagy Regulator BECN1 Following Phosphorylation by STK4/MST1

DOI: 10.1080/15548627.2018.1564557

View abstract
Genes and Development

Physiological Restraint of Bak by Bcl-xL Is Essential for Cell Survival

DOI: 10.1101/gad.279414.116

View abstract

Our team

Meet our researchers

  • A/Prof Doug Fairlie - Head, Cell Death And Survival Laboratory  Publications
  • Erinna Lee - Postdoctoral Research Fellow Publications
  • Tiffany Harris - Research Assistant
  • Nikita Steinohrt - Research Assistant
  • Sharon Tran - PhD Student