A new study has found that cyclin D1, a protein that helps push a replicating cell through the cell cycle also mediates the processing and generation of mature microRNA (miRNA).

The research suggests that a protein strongly implicated in human cancer also governs the non-protein-coding genome.

The non-coding genome, previously referred to as junk DNA, makes up most of the human genome, and unlike the coding genome, varies greatly between species.

"In addition to its role in regulating the cell cycle, cyclin D1 induces Dicer and thereby promotes the maturation of miRNA," lead researcher Richard Pestell, M.D., Ph.D., Director of the Kimmel Cancer Center at Thomas Jefferson University and Chair of the Department of Cancer Biology, said.

Dicer is a protein that converts inactive hairpin-structured microRNA precursors into their active single stranded form.

"The work supports the idea that cancer-causing proteins like cyclin D1 may drive cancer progression in part via miRNA biogenesis," he said.

Using antisense RNA, Dr. Pestell's group was the first to show that cyclin D1 drives mammary tumor growth in vivo.

In prior work, they showed that cyclin D1 regulates the non coding genome, and that the non-coding genome, in turn, regulates expression of cyclin D1.

Furthermore, the group showed that many cancer patients encode a form of cyclin D1 that evades negative feedback from the non coding genome.

These attenuating feedback loops between the non-coding and coding genome may be a common theme in cancer and other biological processes.

In the current study, the group sought to investigate the mechanism by which cyclin D1 regulates the biogenesis of non coding miRNA.

Dr. Pestell and colleagues developed transgenic mice that could induce cyclin D1 expression in the breast and examined cells with cyclin D1 gene deleted.

The researchers noticed that cells lacking cyclin D1 produced less of the miRNA-processing protein, Dicer, and therefore had reduced levels of mature miRNA.

The study is published in the journal Nature Communications.

A new study has found that women who are members of families with BRCA2 mutations but who test negative for the family-specific BRCA2 mutations are still at greater risk for developing breast cancer compared with women in the general population.

Women with certain mutations in their BRCA1 or BRCA2 genes are at increased risk for breast cancer. However, the study suggested that it may not always be true.

"We found that women who test negative for family-specific BRCA2 mutations have more than four times the risk for developing breast cancer than the general population," Gareth R. Evans from University of Manchester in the United Kingdom, said. "We also found that any increased risk for breast cancer is largely limited to BRCA2 families with strong family history and other genetic factors.

Evans said that it is likely that these women inherit genetic factors other than BRCA-related genes that increase their breast cancer risk. About 77 single nucleotide polymorphisms are linked to breast cancer risk.

He said that identification of additional SNPs is necessary to understand why some of the BRCA-negative women from BRCA families are at higher risk.

The authors noted that specialists should use caution when stating that a woman's breast cancer risk is the same as that of the general population following a negative test, because it may not be true for some women who come from BRCA2 families with a strong family history.

The study is published in journal Cancer Epidemiology, Biomarkers and Prevention.