by A groundbreaking study conducted by Tulane University has shed light on a previously unknown molecular pathway that could play a crucial role in halting the progression of lung cancer. Lung cancer remains one of the most prevalent forms of cancer globally, accounting for a significant number of cancer-related deaths worldwide. However, the recently published research in the Proceedings of the National Academy of Sciences holds promise for the development of targeted anti-cancer drugs and personalized treatment approaches for lung cancer patients. Dr. Hua Lu, the Reynolds and Ryan Families Chair in Translational Cancer at the Tulane University School of Medicine and senior study author, explains the significance of the study’s findings.
The research uncovered the potential of a tumor suppressor protein called RBM10 to inhibit the growth of lung cancer by suppressing the activity of c-Myc—a protein known to drive the growth and proliferation of cancer cells that are overexpressed. The study revealed that RBM10 collaborates with two ribosomal proteins, RPL5 and RPL11, to disrupt c-Myc and impede the spread of lung cancer. These findings represent a groundbreaking discovery and establish a previously unknown relationship between these proteins in inhibiting cancer development.
Dr. Lu elaborates on the mechanism through which this protein complex can potentially halt the progression of lung cancer. He likened two cellular factories responsible for manufacturing protein components to the process occurring within a cell. Among these components, c-Myc plays a vital role in protein production and cell growth, which is essential for human survival. However, when cancer cells emerge, they harness the power of c-Myc to sustain their rapid growth, resulting in the accumulation of abnormal protein components that form tumors. RBM10, in partnership with RPL5 and RPL11, has the ability to disrupt c-Myc and arrest tumor growth.
Importantly, the researchers also identified a mutant form of RBM10, prevalent in lung cancer cases, which loses its ability to suppress c-Myc and fails to bind to the ribosomal proteins RPL5 and RPL11. Instead, this mutant form ends up promoting tumor growth rather than inhibiting it. Dr. Lu emphasizes the significance of this finding, explaining that cancer cells mutate RBM10 to block its tumor-suppressing function.
Moving forward, Dr. Lu intends to delve deeper into the function of the RBM10 mutant, hoping to develop an anti-cancer drug specifically targeting it. Designing a molecule that specifically targets this mutant form holds promise as it possesses a unique structure not found in normal tissue. By converting this mutant form, researchers aim to suppress the cancer-causing activity of c-Myc.
Dr. Lu concludes by emphasizing the incremental progress being made toward unraveling the complex molecular mechanisms involved in cancer. Through studies like this, the scientific community is gaining a better understanding of the molecules at play, gradually bringing us closer to more effective treatments for cancer.
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1. Source: Coherent Market Insights, Public sources, Desk research
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