Mayo Clinic researchers reprogramme cancer cells back to normal
Join Our Newsletter - Get important industry news and analysis sent to your inbox – sign up to our e-Newsletter here
X

Mayo Clinic researchers reprogramme cancer cells back to normal

25 Aug 2015

Researchers from Mayo Clinic in the US have discovered a new way to reprogramme cancer cells back to normal, minimising the tumour growth.

Mayo

Researchers from Mayo Clinic in the US have discovered a new way to reprogramme cancer cells back to normal, minimising the tumour growth.

According to Mayo Clinic Florida campus department of cancer biology chair and study senior investigator Dr Panos Anastasiadis, the finding represents, "an unexpected new biology that provides the code, the software for turning off cancer."

The researchers discovered a glue that interacts with the microprocessor and plays a crucial role in the production of molecules called microRNAs (miRNAs), which organise whole cellular programmes through simultaneously regulating expression of a group of genes.

The investigators determined that when normal cells come in contact with each other, a specific subset of miRNAs inhibits genes that promote cell growth.

These miRNAs are misregulated and cells grow out of control, when adhesion is interrupted in cancer cells.

In laboratory experiments, the researchers demonstrated that restoring the normal miRNA levels in cancer cells can reverse that deviate cell growth.

Study lead author Dr Antonis Kourtidis said: "The study brings together two so-far unrelated research fields, cell-to-cell adhesion and miRNA biology, to resolve a long-standing problem about the role of adhesion proteins in cell behaviour that was baffling scientists."

"An unexpected new biology that provides the code, the software for turning off cancer."

The conflicting reports about E-cadherin and p120 catenin have made researchers to carry out study. These adhesion proteins are essential to form normal epithelial tissues and are considered to be tumour suppressors.

Dr Anastasiadis said: "However, we and other researchers had found that this hypothesis didn’t seem to be true, since both E-cadherin and p120 are still present in tumour cells and required for their progression."

The researchers also studied a new protein called PLEKHA7 that associates with E-cadherin and p120 only at the top, or the "apical" part of normal polarised epithelial cells.

They found that PLEKHA7 maintains the normal state of the cells through a set of miRNAs, by attaching the microprocessor to E-cadherin and p120. At this stage, E-cadherin and p120 exert their good tumour suppressor sides.


Image: The study’s lead authors Dr Panos Anastasiadis and Dr Antonis Kourtidis. Photo: courtesy of Mayo Clinic.