Scientists at the BRIC-Rajiv Gandhi Centre for Biotechnology (BRIC-RGCB), Kerala, are developing a new class of drugs aimed at preventing dormant cancer cells from reactivating and triggering cancer recurrence. The research focuses on stopping these inactive cells from transforming into aggressive cancer stem cells (CSCs), which are often responsible for tumour relapse and resistance to treatment.
Discovery Opens New Therapeutic Possibilities
The study, led by Dr. Tessy Thomas Maliekal and published in the peer-reviewed journal Cell Communication and Signaling, has identified a previously unknown reverse-signalling mechanism in the Eph-Ephrin pathway. The researchers found that Ephrin-B1 acts as an oncogenic ligand in cancer stem cells, making it a promising therapeutic target for preventing oral cancer recurrence.
According to the researchers, this signalling mechanism differs from that of normal stem cells and could pave the way for more effective anti-cancer therapies. As per the press release, although the research primarily focuses on oral cancer, similar biological mechanisms may also exist in other cancers and normal stem cell systems.
Blocking Protein Interaction to Prevent Relapse
Dr. Beena Pillai, Director of BRIC-RGCB, said the team has identified an unusual interaction between the proteins EPHA2 and Ephrin-B1 that appears to disrupt normal cellular balance.
“The unusual interaction between EPHA2 and Ephrin-B1 may disrupt cellular balance, creating opportunities for new treatments that target this interaction,” she said.
She added that researchers are currently designing drugs to block this abnormal protein communication. “By preventing this interaction, we aim to stop dormant cancer cells from reawakening and becoming dangerous again,” she explained.
Understanding Why Cancer Returns
Dr. Tessy Thomas Maliekal said the laboratory is investigating what causes dormant cancer cells to resume growth after remaining inactive.
“We study the signals that trigger dormant cancer cells to reprogramme and begin dividing again, and whether these signals can be blocked,” she said.
According to the researchers, dormant cancer cells respond to both their internal properties and external signals from the surrounding microenvironment, including neighbouring cells and chemical messengers. The team found that the abnormal interaction between EPHA2 and Ephrin-B1 specifically occurs in reactivating cancer cells and plays a key role in oral cancer recurrence.
The discovery is considered significant because cancer stem cells are widely recognised as the primary drivers of tumour relapse and resistance to conventional therapies. By targeting this newly identified signalling pathway, researchers hope to develop treatments that reduce the risk of cancer returning after successful therapy.
