A new Tel Aviv University study pinpoints the inverse correlation between a known oncogene; a gene that promotes the development of cancer and the expression of oncosuppressor microRNA as the reason for extended pancreatic cancer survival.
The Scientists examined pancreatic cancer cells and discovered an inverse correlation between the signatures of miR-34a, a tumor suppressant, and PLK1, a known oncogene.
The levels of miR-34a were low in pancreatic cancer mouse models, while the levels of the oncogene were high. This correlation made sense for such an aggressive cancer.
Survival rates in pancreatic cancer linked to the inverse correlation between specific oncogene and tumor suppressant.
The scientists performed RNA profiling and analysis of samples taken from pancreatic cancer patients. The molecular profiling revealed the same genomic pattern found earlier in mouse models of pancreatic cancer.
The scientists then devised a new nanoparticle that selectively delivers genetic material to a tumor and prevents side effects in surrounding healthy tissues.
A nanocarrier is designed to deliver two passengers: (1) miR-34a, which degrades hundreds of oncogenes; and (2) a PLK1 small interfering RNA (siRNA) that silences a single gene. This nanoparticle is like a taxi carrying two important passengers.
The nanocarrier is injected directly to the tumor site to change the molecular signature of the cancer cells, rendering the tumor dormant or eradicating it altogether.
The scientists in order to validate the conclusions they have injected the novel nanoparticles into pancreatic tumor-bearing mice.
Scientists observed that by balancing these two targets; bringing them to a normal level by increasing their expression or blocking the gene responsible for their expression they significantly prolonged the survival of the mice.
This treatment takes into account the entire genomic pattern, and shows that affecting a single gene is not enough for the treatment of pancreatic cancer or any cancer type in general.
