The presence of extra-chromosomal telomeric repeat (ECTR) DNA could suppress alternative lengthening of telomeres (ALT) in cancer cells, Academia Sinica member Chen Liuh-Yow (陳律佑) told a news conference on Tuesday last week.
Cancer cells can be divided into two major groups: those with telomerase and the ALT cancer cells without telomerase, Chen said.
ALT cancer cells comprise 10 to 15 percent of all tumor tissue and are mostly seen in brain tumors in children, as well as soft tissue tumors and bone cancer, Chen said.
ALT cancer cells carry a type of ECTR DNA, which under normal circumstances is tasked with detecting cell-free DNA in activated cells, Chen said.
The process issues interferons that help suppress the diseased cells, Chen said, adding that cancer cells grow because the cells do not have activated interferons.
ECTR DNA does not active interferons in cancer cells because the stimulator of interferon genes (STING) protein is suppressed, Chen said, adding that the inactive histone H3.3 in ALT cancer cells also plays a key role in releasing interferons.
If there is a way to simultaneously repair or restore functions of the STING protein and histone H3.3, it could restore function to the dormant ECTR DNA in cancer cells and prompt the release of interferons to suppress cancer cells, Chen said.
The discovery sheds new light on possible new methods for cancer treatment, Chen said.
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