A research team led by Manel Esteller belonging to the Recerca Biomèdica de Bellvitge Institute (Idibell) has identified a substance – enoxacine – which inhibits the growth of cancerous tumours.
The study will be published this week in the scientific journal ‘Proceedings of the National Academy of Science’ (PNAS).
According to Idibell the research team has identified a substance which inhibits the growth of cancer cells through the activation of the so called dark genome (or non- codified DNA) and micro-ARN molecules.
Human cells possess a genome which codifies our proteins like keratin contained in skin cells or haemoglobin in blood cells.
This genome with codified DNA only represents 5% of our genetic material and the remaining 95% is known as dark genome or non-codified DNA whose function is largely unknown.
A part of this DNA produces small molecules called micro-ARN which have the function of activating or deactivating our genes.
Over the last few years it has been demonstrated that alterations in these molecules are connected to the formation of tumours.
The research team, led by Manel Esteller, has been able to demonstrate that a small molecule enoxacine used in compound antibacterials connects with a protein which makes up micro-ARN and stimulates its inhibiting activity in the growth of a tumour.
Manel Esteller says that ‘its effect is like putting in a newly manufactured engine into a second hand car’.
According to Esteller, it has been tried both in laboratory cells as well as in animals and now its function on humans needs to be studied. Esteller says that the advantage of this compound is that its metabolism and safety for use with humans is already known.
Esteller says that ‘although this molecule might not be used for the treatment of cancer its discovery presents new ways of developing drugs which use micro-ARN as its target’.
Finally Esteller says that ‘we are showing the pharmaceutical industry a new direction towards where it needs to place its efforts in the development of anti-cancer treatments’.