Researchers at the University of Connecticut and Yale University have made significant progress in the treatment of glioblastoma, a particularly lethal and aggressive form of brain cancer.
A new treatment system targets oncogenic microRNAs, referred to more commonly as oncomiRs. These small, shorter strands of RNA not only play a critical role in gene expression, but are also overexpressed in many forms of cancer.
Many forms of modern cancer treatment target miR-21, an oncomiR that displays irregularly high expression in a variety of tumor types, including breast cancer, ovarian cancer and lung cancer, according to Science Direct.
According to 2016 research on microRNA expression published in the National Library of Medicine, hundreds of microRNAs had been identified for their role in the progression of breast cancer, with regulatory modules of microRNA and messenger RNA contributing heavily to the biological processes that drive cancerous development.
The team from the University of Connecticut and Yale University not only targeted miR-21 but also miR-10b, another prominent oncomiR connected to the development of cancers and progressive diseases when dysregulated.
Test mice received a treatment that attached synthesized peptide nucleic acids to miR-10 and miR-21 oncomiRs. The targeting of two oncomiRs instead of one was a relatively unique strategy, but a two-pronged approach succeeded in extending the lifespan of test mice with cancerous cells. On a human level, targeting of multiple oncomiRs could help personalize successful treatments for certain patients, depending on the makeup of one’s tumor.
Yale professor Mark Saltzman and UConn professor Raman Bahal, interviewed in UConn Today, were both optimistic about further application of the group’s research. “These results are the best I’ve ever seen in this sort of aggressive brain tumor,” remarked Saltzman.
University of Connecticut-led team uncovers accelerated aging in depressed adults
A team of researchers led by University of Connecticut School of Medicine student Emma Mastrobattista and associate professor Breno S. Diniz have uncovered irregularly aging mitochondria in depressed adults over 70, which contribute to decreased energy and rapid biological aging.
Mitochondria not only power our cells but our entire bodies. This means that when mitochondrial function decreases, either through poorly functioning protein production or by the aging of the mitochondria itself, energy, strength and mood will decline as well.
The research team has not directly experimented yet with reversing aging in the mitochondria, but the study conducted, the largest of its type, provides a clear link between major depression and accelerated aging, not just in the mitochondria but in cells throughout the body.
According to a 2010 publication in the National Library of Medicine, individuals suffering from depression will also suffer from an increased likelihood to contract various diseases of aging, such as dementia, metabolic syndrome and diseases associated with the cardiovascular system.
Research in Science Direct on stress-induced biological aging has similar findings.
“Stressful life experiences, when occurring repeatedly or over a prolonged period, may accelerate the rate at which the body ages,” the researchers conclude.
Interviewed in UConn Today, Diniz corroborates this assessment of depression as contributing to accelerated aging in cells across the body.
“We have seen it in immune cells, in glial cells… in adipose tissue,” Diniz explains.
The University of Connecticut-led study and others like it on the impact of depression furthers a re-conceptualization of depression as not just a series of feelings or even solely a mental illness. Major depression is a disease that grips not just our minds but our entire bodies.
Pharmacy Researchers Develop Treatment for Glioblastoma – UConn Today
Mitochondria Linked to Major Depression in Older Adults – UConn Today