Chaos Enzyme: Cancer Spread Breakthrough?
- Triple negative breast cancer (TNBC) is one of the most aggressive and hardest forms of breast cancer to treat, but a new study led by Weill Cornell Medicine...
- Triple-negative breast cancer (TNBC) accounts for approximately 10-15% of all breast cancers. it receives this designation because it lacks expression of the three most common receptors - estrogen...
- The study,published in Cancer Discovery,challenges conventional wisdom in cancer treatment.
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Targeting EZH2 Enzyme Shows Promise in Blocking Aggressive Triple-Negative Breast cancer Spread
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Triple negative breast cancer (TNBC) is one of the most aggressive and hardest forms of breast cancer to treat, but a new study led by Weill Cornell Medicine suggests a surprising way to stop it from spreading. Researchers have discovered that an enzyme called EZH2 drives TNBC cells to divide abnormally, which enables them to relocate to distant organs. The preclinical study also found drugs that block EZH2 could restore order to dividing cells and thwart the spread of TNBC cells.
The challenge of Triple-Negative Breast Cancer
Triple-negative breast cancer (TNBC) accounts for approximately 10-15% of all breast cancers. it receives this designation because it lacks expression of the three most common receptors – estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). This absence limits treatment options, as therapies targeting these receptors are ineffective. Consequently, TNBC frequently enough presents a more aggressive disease course and poorer prognosis compared to other breast cancer subtypes.
A New Approach: Restoring Order to Cell Division
The study,published in Cancer Discovery,challenges conventional wisdom in cancer treatment. Traditionally, manny therapies aim to overwhelm cancer cells with further chromosomal instability, pushing them past a point of no return and inducing cell death. However, Dr. Vivek Mittal, the senior author, expresses concern that this approach could paradoxically fuel aggressive disease if the instability isn’t sufficient to kill the cells.
Instead, the Weill Cornell Medicine team found that targeting the enzyme EZH2, a key regulator of gene expression, could restore order to cell division. EZH2 is part of a protein complex called PRC2, which plays a crucial role in epigenetics - changes in gene expression that don’t involve alterations to the underlying DNA sequence. In TNBC cells,EZH2 appears to drive abnormal cell division,facilitating metastasis.
“Metastasis is the main reason patients with triple negative breast cancer face poor survival odds,” said dr. Mittal, Ford-Isom Research Professor of Cardiothoracic Surgery and member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine. “Our study suggests a new therapeutic approach to block metastasis before it starts and help patients overcome this deadly cancer.”
Chromosomal Instability and the Metastatic Potential
Normal cell division relies on precise duplication and separation of chromosomes. However, in many cancer cells, this process becomes chaotic, leading to chromosomal instability – an abnormal number or structure of chromosomes. The researchers discovered that TNBC cells with high metastatic potential exhibit a specific pattern of chromosomal instability driven by EZH2 activity.
Approximately 5% of cells within a primary TNBC tumor are responsible for the vast majority of metastasis. These cells display distinct characteristics, including altered metabolism and increased chromosomal instability. The study suggests that EZH2 is a key driver of this instability in these highly metastatic cells.
The team’s research indicates that blocking EZH2 can correct the errors in cell division, reducing the likelihood of these cells spreading to distant organs.This finding is notable as it suggests a way to target the root cause of metastasis, rather than simply trying to kill already-spreading cells.
The Role of Epigenetics in Cancer Progression
Epigenetics is increasingly recognized as a critical factor in cancer progress and progression. Unlike genetic mutations, epigenetic changes are