Discovery of potential new Eye Tumor treatment

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New research by a team including several Carnegie scientists shows that a specific small RNA segment of an important role in the growth of a type of malignant tumor childhood eye called Retinoblastoma can play. The tumor is associated with mutations of a called Rb or Retinoblastoma protein. Dysfunctional Rb is also involved in other types of cancer, including lung, brain, breast and bot. Their work, which will be the cover story of the August 15th issue of genes & development, can result in a new therapeutic target for the treatment of this rare form of cancer and as well as possible other forms of cancer.

MicroRNAs are a short, single strands of genetic material that bind to longer strands of messenger RNA--that the courier that brings the genetic code of the DNA in the nucleus of the cell Ribosome, where it is translated into protein. This binding activity can microRNAs to silence of the select expression of genes in a targeted manner. Abnormal versions of microRNAs are involved in the growth of different types of cancer.

The paper of the Carnegie Karina Conkrite, Maggie Sundby and David MacPherson-as well as authors from other institutions – focuses on a cluster of called microRNAs miR-17 ~ 92. Recent research has shown that different versions of this cluster are involved in the prevention of pre-cancer cells from dying and allowing them to distribute in tumors. Previous work has shown that miR-17 ~ 92 can be involved in the survival of lymphoma and leukemia cells, by lowering the concentrations of a tumor-suppressing called PTEN.

The team's new research shows that miR-17 ~ 92 may also be involved in retinoblastoma, although it is not in the same way, via the PTEN protein acts, as well as in other types of cancer. Previously, miR-17 ~ 92 acts to help cells that lack tumor suppressing the Rb protein to spread.

First the team shown that miR-17 ~ 92 is expressed in higher-than-usual quantities in all human retinoblastomas examined retinoblastomas, and in some of the mouse. The authors designed mice to express high levels of miR-17 ~ 92 in their retina. When coupled with inactivation of Rb family members, expression of miR-17 ~ 92 led to extremely fast and aggressive Retinoblastoma. Then they showed that this plethora of miR-17 ~ 92 acts to suppress an inhibitor of proliferation, called p21Cip1, which is supposed to compensate for the loss of the Rb.

"These findings-which shows that miR-17 ~ 92 overcomes the cell attempts to compensate for the loss of the Rb-could be similar in other forms of cancer," MacPherson said. "This cluster microRNA could represent a new therapeutic target for the treatment of tumors caused by Rb deficiency."

Article reference:
Carnegie Institution