Scientists have found that the loss of the PDCD4 protein affects cell adhesion – how cells interact and attach with neighbouring cells and structures – which could make it easier for cancer cells to detach and metastasise.
PDCD4 (Programmed Cell Death Protein 4) is a well-documented tumour suppressor – a protein that helps prevent cells from becoming cancerous - and RNA-binding protein. When PDCD4 levels drop, cells are more likely to grow uncontrollably and has been linked to poor outcomes in many cancers.
To understand more fully how dysregulation of this protein can contribute to carcinogenesis, researchers in the Willis lab at the MRC Toxicology Unit studied the function of PDCD4 in normal, healthy cells. They tracked where PDCD4 is located within the cell, which RNAs it binds to and what happens when the protein is depleted.
Interestingly, the team found that PDCD4 binds to RNA molecules that encode for proteins that help cells to maintain their shape, adhere to each other and remain firmly attached to the surrounding environment – a process with major implications for cancer spread.
Furthermore, when PDCD4 levels were reduced, those cells adhered more slowly and less strongly to surrounding surfaces and structures – a behaviour that, in a tumour, could make it easier for cancer cells to detach and spread.
Dr Veronica Dezi, postdoctoral researcher in the Willis lab and first author of the study explained; “This work demonstrates a previously undescribed role for PDCD4 in maintaining cell adhesion in normal, healthy tissues. By studying this protein in ‘normal’ cells, it also provides a new perspective for how PDCD4 acts as a tumour suppressor – which is crucial to understanding how this group of proteins act generally - and additional explanation for poor cancer prognosis in patients with low PDCD4 expression.”
The study ‘Functional characterisation of tumour suppressor PDCD4 reveals previously undisclosed role in the control of cell adhesion’ was published in Nucleic Acids Research on 2nd February 2026. Read the full publication here.