Hai initially discovered worse outcomes in a group of nearly 300 breast cancer patients where the ATF3 gene had been turned on.
Turning on the ATF3 gene is all about stopping the spread of cancer.
Transcription factor ATF3 links host adaptive response to breast cancer metastasis.
Primer NF[kappa]B NM_199267 5'-GTCTCAAACCAAACAGCCTCAC-3' 5'-CAGTGTCTCTTCCTCGACATGGAT-3' TNF[alpha] NM_012675 5'-GTTTCAGTTCTCAGGGTCCTA-3' 5'-CAGGATTCTGTGGCAATCTGG-3' ATF3
NM_012912 5'-CATCAGACCTGATTTCCGAGAGT-3' 5'-AACAGTTTGTAGCCAAGGACAGC-3' Gene Probe NF[kappa]B CCCCAAGCCAGCACCCCAGCCCTAT TNF[alpha] AAAGGGATGAGAAGTTCCCAAATGG ATF3
ACGCGTGCGAAAGAGCCCACCTGAAT The first primer listed is the forward primer, whereas the second primer listed in the reverse primer.
According to the researchers, the study suggests this gene, called ATF3, may be the crucial link between stress and cancer, including the major cause of cancer death - its spread, or metastasis.
Researchers already know that ATF3 is activated, or expressed, in response to stressful conditions in all types of cells.
Under typical circumstances, turning on ATF3 can actually cause normal and benign cells to commit suicide if the cells decide that the stressors, such as irradiation and a lack of oxygen, have irrevocably damaged the cells.
This research suggests, however, that cancer cells somehow coax immune-system cells that have been recruited to the site of a tumor to express ATF3.
Though it's still unclear how, ATF3 promotes the immune cells to act erratically and give cancer an escape route from a tumor to other areas of the body.
Hai and colleagues first linked the expression of the ATF3 gene in immune-system cells to worse outcomes among a sample of almost 300 breast-cancer patients.
The first contains members of the Jun, Fos, and ATF subgroups of transcription factors (C-FOS, FOSB, C-JUN, JUNB, ATF3
, ATF4, ATF5) that form AP-1 dimers implicated in the regulation of cell proliferation and survival (Shaulian and Karin 2001).