How to save the lives of people with cancer who are not cured
30% of people with cancer die from the exhaustion of the body - cachexia. Cachexia is associated with the inhibition of energy metabolism in adipose and muscle tissues. The tumor rebuilds the functioning of the nervous, immune systems, and metabolism. Moreover, cachexia depletes the body so much that the patient does not tolerate infection and damage, the toxic effects of treatment. As a result, the organs of a person with cachexia fail.
Introduction
The fact is that tumor cells divide actively and are similar to the tissue that regenerates after injury. When the body recovers from damage, a series of signals switches it into a passive state. Due to reduced appetite, the animal does not go out to search for food, and this saves the weakened body from predators. At the same time, a supply of nutrients is consumed for recovery. Normally, this ends with recovery. But often tumor cells exploit repair-oriented processes without stopping. Apparently, this is how cachexia develops. This means that in order to help patients exhausted by cachexia, it is necessary to find a way through which the tumor inhibits the work of the body.
Perplexed by the search, biologists found that the signal of BMPs proteins resists the inhibitory effect of the tumor.
BMPs, Bone morphogenetic proteins, during the development of the embryo, affect the laying of the skeleton, which cell will give rise to this or that tissue, that is, they determine the structure of the body. In an adult, BMPs are the main regulators of bone and cartilage regeneration, that is, they also trigger tissue growth.
When the membrane receptor transmits the BMPs signal into the cell, SMAD proteins are activated, which move to the cell nucleus to rearrange its work. Among other things, the BMPs signal stimulates muscle growth when there is a lot of protein - muscle growth is even excessive. This maintains the life of muscle cells in conditions of insufficient innervation. But, according to previous research, the noggin protein blocks the BMPs receptor.
Results
The researchers turned their attention to the noggin. And they found that its synthesis is stimulated by interleukin-6 (IL-6) and activin A, which immune cells produce due to the tumor. As a result of the overproduction of noggin, the muscles of the experimental mice were not only exhausted, but also lost contact with the motor neurons that control the muscles. After all, the neuromuscular connection is reinforced only when needed. Scientists studied the muscles of cancer patients with cachexia and saw the same problems as in the muscles of mice: excess noggin, signs of denervation, and atrophy.
After confirming the link between cachexia and noggin, the scientists tried to treat mice at risk of cachexia with tilorone, an amplifier of BMPs signaling in lung cells. Tiloron helped: restored the work of motor neurons and stopped weight loss. The drug even increased the survival rate of mice, although it had no effect on tumor growth. Perhaps the therapeutic effect of tilorone is also associated with its anti-inflammatory action and IL-6.
The medicinal effect of tilorone in relation to cachexia will be studied further. Keeping cancer patients healthy is just as important as treating their disease. ChemDiv's Anticancer Library can help the researcher on the path to either of these two goals. This library will allow you to design many experiments with different effects on cancerous tumors. You can read more about the Anticancer Library here https://www.chemdiv.com/catalog/focused-and-targeted-libraries/anticancer-library/.
Alexander Khazanov
References
Sartori, Roberta, et al. "Perturbed BMP signaling and denervation promote muscle wasting in cancer cachexia." Science Translational Medicine 13.605 (2021): eaay9592.
Introduction
The fact is that tumor cells divide actively and are similar to the tissue that regenerates after injury. When the body recovers from damage, a series of signals switches it into a passive state. Due to reduced appetite, the animal does not go out to search for food, and this saves the weakened body from predators. At the same time, a supply of nutrients is consumed for recovery. Normally, this ends with recovery. But often tumor cells exploit repair-oriented processes without stopping. Apparently, this is how cachexia develops. This means that in order to help patients exhausted by cachexia, it is necessary to find a way through which the tumor inhibits the work of the body.
Perplexed by the search, biologists found that the signal of BMPs proteins resists the inhibitory effect of the tumor.
BMPs, Bone morphogenetic proteins, during the development of the embryo, affect the laying of the skeleton, which cell will give rise to this or that tissue, that is, they determine the structure of the body. In an adult, BMPs are the main regulators of bone and cartilage regeneration, that is, they also trigger tissue growth.
When the membrane receptor transmits the BMPs signal into the cell, SMAD proteins are activated, which move to the cell nucleus to rearrange its work. Among other things, the BMPs signal stimulates muscle growth when there is a lot of protein - muscle growth is even excessive. This maintains the life of muscle cells in conditions of insufficient innervation. But, according to previous research, the noggin protein blocks the BMPs receptor.
Results
The researchers turned their attention to the noggin. And they found that its synthesis is stimulated by interleukin-6 (IL-6) and activin A, which immune cells produce due to the tumor. As a result of the overproduction of noggin, the muscles of the experimental mice were not only exhausted, but also lost contact with the motor neurons that control the muscles. After all, the neuromuscular connection is reinforced only when needed. Scientists studied the muscles of cancer patients with cachexia and saw the same problems as in the muscles of mice: excess noggin, signs of denervation, and atrophy.
After confirming the link between cachexia and noggin, the scientists tried to treat mice at risk of cachexia with tilorone, an amplifier of BMPs signaling in lung cells. Tiloron helped: restored the work of motor neurons and stopped weight loss. The drug even increased the survival rate of mice, although it had no effect on tumor growth. Perhaps the therapeutic effect of tilorone is also associated with its anti-inflammatory action and IL-6.
The medicinal effect of tilorone in relation to cachexia will be studied further. Keeping cancer patients healthy is just as important as treating their disease. ChemDiv's Anticancer Library can help the researcher on the path to either of these two goals. This library will allow you to design many experiments with different effects on cancerous tumors. You can read more about the Anticancer Library here https://www.chemdiv.com/catalog/focused-and-targeted-libraries/anticancer-library/.
Alexander Khazanov
References
Sartori, Roberta, et al. "Perturbed BMP signaling and denervation promote muscle wasting in cancer cachexia." Science Translational Medicine 13.605 (2021): eaay9592.
