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Deutsch (EUR)09. Apoptosis and Cancer: How the Body Removes Damaged Cells
09 · Apoptosis and Cancer: How the Body Removes Damaged Cells
Apoptosis is a regulated process through which the body removes unwanted or damaged cells. It helps maintain tissue balance and is one of the mechanisms that protect against tumour development.
This article explains the roles of mitochondria, the p53 protein and caspases, as well as why cancer cells can sometimes evade this process. [1]
What is apoptosis?
Apoptosis is often described as programmed cell death. A cell activates a sequence of molecular steps that lead to its orderly breakdown and removal. It is a natural part of development and tissue renewal. It does not automatically indicate disease. [1]
The intrinsic pathway: mitochondria and cell damage
During severe cellular stress, the proteins BAX and BAK can increase the permeability of the outer mitochondrial membrane. Molecules are then released from the mitochondria, including cytochrome c. Proteins that promote cell survival, such as BCL-2, also influence the balance of this pathway. [2]
It participates in electron transfer in the respiratory chain.
In the cytoplasm, it can help assemble an apoptotic signalling complex.
Together with the protein APAF-1, it helps form a complex called the apoptosome. This activates caspase-9 and subsequently the executioner caspases, particularly caspases-3 and -7. This mitochondrial pathway of apoptosis has been extensively studied. [3]
p53: a protein involved in the response to DNA damage
TP53 is a gene; p53 is the protein produced using its instructions. When DNA is damaged, p53 helps regulate cell division, damage repair and, under certain circumstances, apoptosis. This is why it is known as the “guardian of the genome”.
Not all DNA damage leads to cell death. The response depends on the extent of the damage and the cellular context. Changes in the TP53 gene occur in many cancers, but their frequency varies considerably between cancer types. [4]
The extrinsic pathway: signals through receptors
Apoptosis can also be triggered by external signals that bind to particular receptors on a cell. Examples include the receptors DR4 and DR5, which bind the signalling molecule TRAIL. TRAIL is therefore not the receptor itself. Activation of this pathway can lead to a caspase cascade. [5]
The intrinsic and extrinsic pathways are not completely separate: their signals can interact and influence a cell’s sensitivity to apoptosis.
Caspases and cell removal
Caspases are enzymes that cleave selected proteins. During apoptosis, they contribute to the orderly breakdown of cellular structures. The cell shrinks, and its contents may be divided into membrane-bound apoptotic bodies. [3]
Phagocytes, such as macrophages, engulf the dying cell and its remnants. Prompt clearance limits the leakage of cellular contents and the inflammatory response. However, it is not accurate to say that apoptosis is entirely free of inflammation under all circumstances. [6]
Apoptosis, necrosis and autophagy: what is the difference?
| Process | What it means |
|---|---|
| Apoptosis | An orderly form of cell death followed by removal of the cell. |
| Necrosis | Cell death accompanied by loss of membrane integrity and leakage of cellular contents; often associated with inflammation. Regulated forms of necrotic cell death also exist. |
| Autophagy | The breakdown and recycling of cellular components, which often help a cell survive. It is not a synonym for apoptosis. |
Why can cancer cells evade apoptosis?
Cancer cells may have weakened mechanisms that would normally lead to their removal. One example is impaired p53 function. Another is an increased dependence on proteins that support survival, such as BCL-2. [4, 7]
A cell may fail to respond appropriately to damaged DNA and continue dividing.
Proteins that inhibit apoptosis can help a cancer cell withstand stress or treatment.
Evading apoptosis is not the same as immortality. It is one of several characteristics that can contribute to tumour survival and growth.
How is apoptosis used in cancer treatment?
Some cancer treatments rely on the ability of cancer cells to undergo apoptosis. One specific example is venetoclax, a medicine that blocks the BCL-2 protein. It is used in selected settings for chronic lymphocytic leukaemia and acute myeloid leukaemia. [7]
It is not a universal treatment for all tumours. Treatment selection depends on the diagnosis, tumour characteristics and the patient’s health. Treatment is managed by a specialist; individual cancer treatments may act through several mechanisms.
What do claims about “substances that trigger apoptosis” mean?
When reading research, it is important to distinguish between experiments on isolated cells, animal studies and clinical studies in humans. Killing cancer cells in a laboratory does not, by itself, demonstrate an effective and safe treatment for people.
This also applies to claims about curcumin, quercetin, EGCG or resveratrol. Results from a cell experiment cannot establish the effectiveness of a dietary supplement against cancer or a recommended anticancer dose.
What matters is whether a substance, when administered safely, demonstrably improves treatment outcomes in patients. Supplements used during cancer treatment also need to be assessed for potential interactions.
Frequently asked questions
Is apoptosis always harmful?
No. It is a natural part of how the body functions and helps remove unwanted or damaged cells. Appropriate regulation is important.
Are apoptosis and autophagy the same?
No. Apoptosis leads to the removal of an entire cell. Autophagy recycles cellular components and often supports cell survival.
Is p53 a gene or a protein?
p53 is a protein. The gene containing the instructions for making it is called TP53.
Does triggering apoptosis in a test tube prove effectiveness against cancer?
No. A laboratory result alone does not establish safety or clinical benefit in humans. These must be tested in clinical studies.
Can a home routine safely trigger apoptosis in cancer cells?
No general home routine can be recommended to safely and selectively remove cancer cells. Cancer treatment must be based on the specific diagnosis.
Sources and further reading
- National Cancer Institute: Apoptosis — definition and relevance to cancer cells.
- Wei et al. (2001): Proapoptotic BAX and BAK — experimental research on the mitochondrial pathway.
- Li et al. (1997): Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex — original mechanistic study.
- MedlinePlus Genetics: TP53 gene — p53 function and changes in cancer.
- Schneider et al. (1997): TRAIL receptors 1 (DR4) and 2 (DR5) — receptor signalling.
- Fadok et al. (1998): Macrophages that have ingested apoptotic cells — a cell experiment on cell clearance and inflammatory signals.
- European Medicines Agency: Venclyxto — approved uses of venetoclax.
