Physicians treating patients with non-small cell lung cancer (NSCLC) may find the following article extremely beneficial. A latest research triggered by the Virginia Commonwealth University Massey Cancer Center has put forth a probable mechanism in non-small cell lung cancer (NSCLC) cells that assist in their capacity to maintain and grow tumors. It was suggested that a protein factor controls the expression of the caspase-9 protein, which is a hallmark in either apoptosis or programmed cell death.
Understanding the newly discovered mechanism seems to be crucial for introducing effective NSCLC therapies. Healthy cells possibly favor caspase-9a that is a type of caspase-9a enhancing natural apoptosis. While conducting the research it appeared that NSCLC cells favor caspase-9b. It is known that caspase-9b is the anti-apoptotic form of caspase-9 promoting tumor formation, growth as well as maintenance. Researchers also observed that the hnRNP L protein functions as a RNA splicing factor by assisting the expression of caspase-9b through a process termed as RNA splicing.
Charles E. Chalfant, Ph.D., associate professor of biochemistry, molecular biology and lead researcher, quoted, “Unfortunately, many current therapies for lung cancer are less effective and more toxic than we’d like. Lung cancer kills more people than any other cancer, and there is a real need for new cellular targets that are cancer-specific and show results in large numbers of patients regardless of the mutations found in individual tumors. Since caspase-9b is mainly expressed in malignant cells, these findings may provide innovative treatments for non-small cell lung cancer with little to no toxic side effects.”
Caspase-9b seems to be a vital target in the development of a durable therapy for non-small cell lung cancer. Experiments on mouse models were conducted with the help of a virus-based targeted gene therapy to decline the amount of hnRNP L in NSCLC cells. A lower ratio of caspase-9b to caspase-9a appeared. As a result, complete halt in the growth of tumors were witnessed with no negative effects on healthy cells. Investigators believe that a reduction in cancer cells’ capacity to maintain tumors can make them more vulnerable to chemotherapy drugs. These medications probably have little effect on NSCLC.
The research was published in Journal of Clinical Investigation.