[ad_1]
Hua-Ying Fan, PhD, is studying the cells of people without cancer. These people have a hereditary disorder called Cockayne Syndrome and, unfortunately, they do not live long enough to develop cancer. But by studying their cells, Fan may be able to help them and help people with cancer.
Fan is a scientist in molecular medicine at the University of New Mexico's Center for Cancer Research. By studying the differences between the cells of people with Cockayne syndrome and those who are not, Fan and his research team have discovered the importance of a protein called CSB.
The cells of people with Cockayne syndrome do not form CSBs. They also have high levels of molecules called reactive species of oxygen. Normal cell functions produce reactive oxygen species, but when they accumulate too much, these molecules damage the cell 's DNA, which causes it to stress and accelerate its death.
Cockayne is a syndrome of premature aging. The cell just died. "
Hua-Ying Fan, Ph.D., Scientist in Molecular Medicine at the Comprehensive Cancer Center of the University of New Mexico
The Fan team discovered that in healthy cells, the CSB protein helps repair DNA damage caused by reactive oxygen species. And they discovered that CSB had to work with another protein called PARP1.
According to Fan, PARP1 goes to where the DNA is damaged, and then attracts CSB to that location. The CSB and PARP1 work together to repair the DNA. None of the proteins can effectively repair the DNA alone.
Fan's team discovered another link between the two proteins.
"When cells are stressed," she says, "a different set of genes needs to be activated, in addition to [those for] housekeeping functions. These gene products must be generated. "
These gene products are proteins that lower the levels of reactive oxygen species when they become too high. Again, PARP1 and CSB combine to transcribe DNA and create proteins that fight the reactive species of oxygen.
Thus, in healthy cells, CSB not only helps to fight against excess reactive oxygen species, but also to repair the damage that they create. The cells of people with Cockayne syndrome are devoid of CSB and can not lower the levels of reactive oxygen species nor repair their damage to DNA.
Fan hopes to use this research to develop ways to make existing cancer drugs more powerful. Anticancer drugs that work by interfering with PARP1 may be a good choice. If resistance to these drugs develops, Fan thinks that preventing the collaboration of CSB and PARP1 could cause faster death of cancer cells.
"There is more motivation to seek inhibitors for CSB," she says.
Fan is eager to discover potential drugs that inhibit BSC in people with cancer – or who take his place – in people with Cockayne Syndrome.
Source:
Comprehensive Cancer Center of the University of New Mexico
Journal reference:
Fan, H. et al. (2018) Poly (ADP-ribose) polymerase 1 (PARP1) promotes the oxidative stress-induced badociation of group B protein from Cockayne syndrome with chromatin. The biological chemistry journal. doi.org/10.1074/jbc.RA118.004548.
[ad_2]
Source link
