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Inhibiting NLK in cancers with mutated PTEN could turn the cancer's strength against it

Inhibiting NLK in cancers with mutated PTEN could turn the cancer's strength against it | Longevity science | Scoop.it

A mutation that allows cells to grow out of control could also provide a new way to target and destroy cancer cells. This potential Achilles’ heel comes from a mutation in a gene called PTEN, which is found in a wide range of cancers.

 

PTEN is one of many tumor suppressor genes that we have to prevent our cells from growing out of control. If the PTEN gene stops working because of a mutation, it can cause tumours to develop – indeed many tumors have a mutated form of PTEN. However when a door closes, a window opens: the PTEN mutation helps the tumor to grow, but it could also mark it out as a target.

 

Researchers from the Institute of Cancer Research, London, found that switching off another gene known as NLK (Nemo-like kinase) killed tumor cells that had the PTEN mutation. This makes NLK a good target for drug developers to create a new cancer treatment.

 

Initially, the researchers took samples of tumor cells with and without the mutation, and switched off genes for important proteins that are used for regulating lots of processes in the cell. To do this they used small interfering RNA (or siRNA) which interfere with the processes of specific genes. These siRNAs block the chain of events that allow a gene to produce a protein, effectively switching it off. By switching off 779 genes individually, they could look for ones where cells with the PTEN mutation died and cells without the mutation survived.

 

This is how the researchers discovered the powerful effect of switching off the NLK gene. They are not certain how this works but it appears to protect a protein called FOXO1 that can act as a backup tumor suppressor and cause the cancer cell to die. When PTEN is mutated, the FOXO1 protein becomes vulnerable to a process called phosphorylation, which means it is ejected from the cell nucleus and destroyed. NLK is one of the proteins that phosphorylates FOXO1 and so by switching off the NLK gene, FOXO1 is able to do its job.

 


Via Dr. Stefan Gruenwald
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Do statins drain your energy?

There is a large population that take 'statin drugs' to lower cholesterol.

 

These drugs are very effective, but can result in muscle pain and fatigue. Why? The drugs deplete the body's natural reserves of CoEnzyme Q10, which is involved in energy production at the cellular level.

 

Fortunately, supplementing with the enzyme can help restore the blood levels and counterract the side effects. But few doctors mention this when they prescribe the drugs.

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Tyk2 enzyme helps regulate obesity through differentiation of brown adipose tissue

Approximately 68 percent of U.S. adults are overweight or obese, according to the National Cancer Institute, which puts them at greater risk for developing cancer, cardiovascular disease, diabetes and a host of other chronic illnesses.

But an international team of scientists led by Virginia Commonwealth University Massey Cancer Center researcher Andrew Larner, M.D., Ph.D., has successfully reversed obesity in mice by manipulating the production of an enzyme known as tyrosine-protein kinase-2 (Tyk2). In their experiments, the scientists discovered that Tyk2 helps regulate obesity in mice and humans through the differentiation of a type of fat tissue known as brown adipose tissue (BAT).
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This discovery may lead to methods to treat obesity by modulating levels of the enzyme. If successful, not only would obesity rates decrease, but healthy life span would increase.

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