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| Stay young, start from the cell |
Cell image source: University of Montreal
Cell image source: University of Montreal Researchers at the University of Montreal and McGill University in Canada have discovered a new multi-enzyme complex that can reprogram the metabolic program to overcome "cell aging", that is, aging cells stop dividing
.
In a study published recently in Molecular Cell, scientists discovered that an enzyme complex called HTC (Hydrogenate Transfer Complex) can inhibit cell senescence
.
"HTC can protect cells from hypoxia, which usually leads to cell death
.
" said Gerardo Ferbeyre, senior author of the study, professor of biochemistry at the University of Michigan, and chief scientist at the research center of the university's teaching hospital
"Importantly, HTC can be hijacked by certain cancer cells to improve their metabolism, resist hypoxic environment and proliferate
.
" Ferbeyre said
HTC is composed of three enzymes: pyruvate carboxylase, malate dehydrogenase-1 and malic enzyme-1
.
They are highly expressed in prostate cancer mouse model samples and tissue samples from prostate cancer patients made by the University of Veterinary Medicine in Vienna, Austria
Most interestingly, Ferbeyre said, inhibiting these enzymes can stop the growth of prostate cancer cells, which suggests that HTC may be a key target for the development of new therapies for various cancers, including prostate cancer
.
"
Most of the key metabolic cycles were discovered more than 50 years ago, but HTC is not among them
.
One of the study authors, McGill University researcher and professor of medicine Ivan Topisirovic said: "We discovered this phenomenon through the most advanced metabolomics analysis
Scientists can assemble enzyme complexes from purified proteins and obtain biophysical data about their composition
.
Their next step will be to generate a detailed high-resolution structure of the enzyme complex in order to design drugs that can modulate its function
Related paper information: https://doi.
https://doi.
org/10.
1016/j.
molcel.
2021.
08.
028 https://doi.
org/10.
1016/j.
molcel.
2021.
08.
028
