A leading researcher from USC is currently working with colleagues from the University of Texas at San Antonio (UTSA) and University of Texas Health Science Center at San Antonio to identify a critical cancer-causing component that leads to AIDS-related cancer. The results have revealed key information in the virus that causes Kaposi’s sarcoma, the most common cancer among HIV-infected people, which will in turn allow researchers to develop new drugs that can help prevent Kaposi’s sarcoma and other related cancers from developing.
S. J. Gao, Ph.D., professor of molecular microbiology and immunology at the Keck School of Medicine of the University of Southern California (USC) and principal investigator of the study, explained exactly what researchers were able to learn in their research: “The mechanism behind the Kaposi’s sarcoma-associated herpesvirus (KSHV) that causes healthy cells to become malignant is not well understood despite two decades of intensive studies,” adding that, “This is the first time that a viral factor has been shown to be required for KSHV-induced malignant transformation. We have identified a mechanism by which these tiny viral molecules cause the cells to become malignant.”
The primary and most common symptom in Kaposi’s sarcoma — the development of dark lesions on the skin — occurs most commonly with those who are infected with KSHV and who have compromised immune systems, such as from the effects of HIV/AIDS. Often times, many people infected with KSHV never show any outward symptoms of the disease. However, in demographics where HIV infection is high and access to HIV drugs is limited, Kaposi’s sarcoma is a persistent problem, easily identified by the lesions. For example, according to a recent press release, “more than 90 percent of the population in some areas of Africa shows signs of KSHV infection, according to the American Cancer Society.”
Gao’s research involved studying KSHV using a rat stem cell model they developed in 2012. Prior to this new test, researchers were never able to study the KSHV virus with any degree of accuracy, since most healthy cells, once infected with KSHV, died before turning into cancer cells.
The new study, which appeared in the December 26th edition of the peer-reviewed journal PLOS Pathogens, outlines how the research team were able to locate “a cluster of viral microRNA molecules that are necessary to transform healthy cells into cancerous ones. When this microRNA cluster was suppressed, the cells died after they were infected with KSHV. Flipping the switch and turning the cluster back “on,” however, allowed the cells to stay alive and become malignant when infected with the virus. Using advanced genomic methods, the researchers also found that the microRNAs target the IκBα protein and the NF-κB cellular pathway, both of which are associated with cancer development.”
Gao went on to explain, “Our results suggest that this cluster of KSHV microRNAs and their regulated NF-κB pathway may be potential targets for new therapeutics of KSHV-related cancers. Several of the microRNAs appear to have redundant functions, so targeting their common pathways might be a more feasible approach. It would be interesting to test them in the KSHV-induced Kaposi’s sarcoma model.”
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