New Delhi, July 3 (IANS) A team of Australian scientists has identified a group of proteins that could transform approaches to treating cancer and age-related diseases.

Researchers at the Children’s Medical Research Institute (CMRI) in Sydney discovered that these proteins play a crucial role in controlling telomerase — an enzyme responsible for protecting DNA during cell division, Xinhua news agency reported.

The breakthrough clarifies how telomerase both supports healthy ageing and fuels cancer cell growth, highlighting new possibilities for treatments that slow ageing or stop cancer by targeting these newly identified proteins, the team said.

Telomerase helps maintain the ends of chromosomes, known as telomeres, which are vital for genetic stability.

Telomerase adds DNA to the ends of chromosomes (telomeres) to protect them from damage.

While telomerase is essential for the health of stem cells and certain immune cells, cancer cells often exploit this enzyme to grow uncontrollably.

CMRI Researchers have now identified a new set of proteins that play a vital role in controlling this enzyme.

In the paper published in the journal Nature Communications, the team highlighted that three proteins — NONO, SFPQ, and PSPC1 — guide telomerase to chromosome ends; disrupting them in cancer cells prevents telomere maintenance, potentially stopping cancer cell growth.

“Our findings show that these proteins act like molecular traffic controllers, making sure telomerase reaches the right destination inside the cell,” said Alexander Sobinoff, the lead author of the study.

“Without these proteins, telomerase can’t properly maintain telomeres, a finding which has significant implications for healthy aging and cancer progression,” Sobinoff added.

Hilda Pickett, head of CMRI’s Telomere Length Regulation Unit and the study’s senior author, noted that understanding how telomerase is controlled opens new possibilities for developing treatments targeting cancer, ageing, and genetic disorders linked to telomere dysfunction.

–IANS

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