Cancer cells exploit cell cycles to multiply rapidly, a process known as proliferation. Cancer drugs aim to halt this growth by initiating a complex sequence of genetic and cellular events. However, these treatments often yield mixed results
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US researchers have found during a study how cancer cells manage to evade despite treatment. Published in the Proceedings of the National Academy of Sciences, the study delves into the cellular processes that allow cancer cells to proliferate even when targeted by anticancer drugs.
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Cancer cells exploit cell cycles to multiply rapidly, a process known as proliferation. Cancer drugs aim to halt this growth by initiating a complex sequence of genetic and cellular events. However, these treatments often yield mixed results.
The team led by Jean Cook of the Department of Biochemistry and Biophysics at University of North Carolina, Chapel Hill, identified a crucial enzyme that plays a key role in stopping cancer cell proliferation, particularly during treatment with anti-cancer drugs.
This enzyme's function varies among individuals. The researchers also discovered mechanisms through which cancer cells evade therapies designed to inhibit them.
Cells regulate protein expression by turning genes "on" and "off".
Some proteins ensure precise and effective cell division, akin to musicians in an orchestra guided by a conductor.
Cells can deactivate these regulatory proteins, allowing uncontrolled division and DNA replication.
To explore protein degradation's role in halting cell growth, Cook and graduate student Brandon Mouery treated cultured human cells with palbociclib, a metastatic breast cancer drug.
Using microscopy, flow cytometry, and proteomics, they found that the enzyme APC/C, which targets proteins for degradation to regulate the cell cycle, enhances the effectiveness of palbociclib.
This finding suggests that APC/C levels in tumours could help predict patient responses to palbociclib and similar drugs.
Reduced APC/C activity might indicate poor treatment response or a higher relapse risk.
The researchers also observed that both cancerous and non-cancerous cells can bypass drug-induced proliferation arrest.
These escapee cells struggle to replicate DNA independently, likely delegating DNA replication to proteins that initiate cell division later in the cell cycle.
This indicates that cells can use alternate pathways for uncontrolled growth.
"Cell proliferation has been intensively studied for decades, yet we can still be surprised," Cook noted. "Sometimes our textbook understanding is still quite incomplete, so we need to keep an open mind and continually challenge paradigms."
These findings could lead to new interventions that induce long-lasting proliferation arrest by exploiting this escape mechanism and cancer-associated DNA replication errors, potentially forcing cancer cells into a "self-destructive" growth mode.
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