New Delhi, Dec. 16: Research led by an Indian scientist in the US has revealed a mechanism previously unknown to science that drives the lethal spread of cancer cells from their primary sites to other tissues.

The experimental work shows how cancer cells hijack normal cells to drive the process called metastasis - the spread of cancer from one part of the body to other parts - which accounts for over 90 per cent of cancer-related deaths.

The observations show that cancer cells construct tiny "molecular nano-bridges" to make connections with and take over the genetic machinery of normal cells and use them to slip into the bloodstream, a key step in metastasis.

"We're seeing cancer cells hijacking normal cells to spread through metastasis - this is the first time something like this has ever been observed," Shiladitya Sengupta, an assistant professor at the Harvard Medical School Brigham Women's Hospital, Boston, who led the study, told The Telegraph.

The findings are expected to pave the way to new strategies to block metastasis, a cascade of events in which the cancer cells invade blood vessels, float in the bloodstream, and spread out to form secondary cancer sites in distant tissues or organs. For breast cancer, the most common sites of metastasis are the brain, liver, lungs and bone.

Sengupta and his colleagues who used powerful microscopes to examine how metastatic breast cancer cells interact with endothelial cells that line the body's blood vessels detected long thin tube-like structures extending from the cancer cells to healthy endothelial cells.

Sengupta and his colleagues have described their findings in a paper published today in the journal Nature Communications.

The researchers hypothesised that the cancer cells use these structures, or nano-scale bridges, to transfer genetic material called micro-RNAs into the endothelial cells - and confirmed this by detecting two micro-RNAs implicated in metastasis in transformed endothelial cells.

"The cancer cells inject micro-RNAs through the nano-scale structures, turning normal cells into pathological cells that facilitate metastasis," said Sengupta, who studied biology and pharmacology at the All India Institute of Medical Sciences, New Delhi, before moving to the University of Cambridge and the US.

For metastasis, the cancer cell transforms healthy endothelial cells, creating gaps in the lining of the blood vessels, he said. The gaps allow cancer cells to move into the bloodstream.

The researchers then used chemical compounds to prevent the formation of the nano-scale bridges, thus disrupting the channels of communication between the cancer cells and the healthy endothelial cells.

They found that a chemotherapeutic drug called docetaxel - which is used to treat metastatic cancer - decreased the number of such bridges.

In mice treated with chemicals that can prevent bridges, the scientists observed a decrease in the metastatic tumour burden.

"We have shown that if you target the building blocks of the nano-scale bridges, you can obstruct metastasis," Sengupta said.

This work provides insights into cell-to-cell communication in tumours, Elazaer Edelman, professor of health science and technology at the Massachusetts Institute of Technology, said in a media release issued by the Brigham Women's Hospital.

"(This) will shed new light on cancer as a disease," he said, adding that knowledge of mechanisms underlying metastasis could also lead to innovative therapies.