Researchers from the University of Michigan Rogel Cancer Center have uncovered a promising new target in the battle against aggressive forms of prostate cancer.
Led by Dr. Joshi Alumkal, the team has identified a protein called lysine-specific demethylase 1 (LSD1) that plays a crucial role in the progression of prostate cancer from a more manageable state to a highly aggressive form.
Prostate cancer is often treatable, especially in its early stages. However, some tumors can evolve into a more dangerous variant known as neuroendocrine prostate cancer.
This transition, driven by a process called lineage plasticity, makes the cancer much harder to treat, leaving patients with limited options. The discovery of LSD1’s involvement in this process is a significant step forward in understanding how and why this transformation happens.
LSD1 is a protein that acts as a switch in the cell, turning certain genes on or off. It is present in both healthy and cancerous cells.
Dr. Alumkal’s previous research had already shown that LSD1 is vital for the survival of prostate adenocarcinoma, a more common type of prostate cancer, by activating genes associated with stem cells.
These latest findings reveal that LSD1 is even more active in neuroendocrine prostate cancer, the more aggressive variant.
To explore LSD1’s role further, the team conducted experiments where they removed LSD1 from neuroendocrine prostate cancer cells. The result was a significant slowdown in cancer growth.
They also found that blocking LSD1’s interactions with other proteins, rather than just stopping its usual enzyme activity, was a more effective way to halt the cancer’s progress.
One of the most exciting parts of this research involves a drug called seclidemstat, an allosteric inhibitor that targets LSD1. This drug is already being tested in phase 1 clinical trials for treating sarcoma, another type of cancer.
In their experiments, Dr. Anbarasu Kumaraswamy and the team found that seclidemstat was not only effective in stopping the growth of prostate cancer cells, but in some cases, it even reversed the growth of the cancer.
Importantly, the drug achieved these results without harming the mice used in the study, suggesting it could be a safe option for human treatment.
Another key finding from the study is related to p53, a gene that plays a vital role in preventing tumor growth. The team discovered that LSD1 deactivates p53, which allows cancer to grow unchecked.
However, when LSD1 was inhibited, p53 was reactivated, leading to a reduction in tumor growth. This discovery opens up the possibility of using LSD1 inhibitors not just in prostate cancer, but potentially in other types of cancer as well, by reactivating p53.
The implications of these findings are significant. Targeting LSD1 with drugs like seclidemstat offers new hope for treating neuroendocrine prostate cancer, which is notoriously difficult to manage.
The potential to reactivate p53 also suggests that this approach could be used in a broader range of cancers.
Dr. Alumkal is hopeful that clinical trials targeting LSD1 for aggressive prostate cancers could start soon, especially since seclidemstat is already being tested in other cancers.
This discovery could lead to a new direction in cancer therapy, focusing on the role of LSD1 in cancer progression.
While the fight against cancer is a challenging one, discoveries like this provide new strategies and hope. By targeting key proteins like LSD1, researchers are paving the way for more effective treatments, not just for prostate cancer, but possibly for other forms of cancer as well.
This progress brings us closer to finding better ways to combat this formidable disease and improve outcomes for patients around the world.
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