ATF3 Inhibits Doxorubicin-induced Apoptosis in Cardiac Myocytes: A Novel Cardioprotective Role of ATF3

Far Infrared Ray Radiation Inhibits the Proliferation of A549, HSC3 and Sa3 Cancer Cells through Enhancing the Expression of ATF3 Gene

“…In contrast, some works demonstrated that ATF3 is anti-apoptotic gene [26,39,40]. Recently, researchers concurred that ATF3 can play both pro-apoptotic and cell survival role depending on the type of stimulation and cell context [21,26,32,36,39]. In our study, there were shown the cell hypertrophy of FIR-sensitive cell lines without apoptosis.…”

“…and protein was peaked at 1 h and 2 h after Doxorubicin treatment in cardiac myocytes [39], ATF3 mRNA is rapidly increased in 30 min after TNF-α stimulation in HUVECs and ATF3 protein was also induced with maximum accumulation in 4 h and involved TNF-α induced HUVECs apoptosis in atherosclerotic region [26,39]. Kawauchi et al, reported that the level of ATF3 increased within 4 h after TNF-α stimulation in HUVECs and protected HUVECs from TNF-α inducible cell death by down-regulating the activity of pro-apoptotic gene p53 [40], ATF3 is induced in ovarian cancer cell lines by progesterone after 4 h of culture [31], the increase in ATF3 mRNA was evident in the earliest time point 4h and was maintained through 24 hours of curcumin treatment in some human cancer cell lines [32].…”

“…Then e propound the hypothesis, that ATF3 as a transcriptional repressor under the continuous expression can inhibit the activity of pro-apoptotic genes such a p53, etc [40] although many studies have shown ATF3 is proapoptotic gene [32,36]. In contrast, some works demonstrated that ATF3 is anti-apoptotic gene [26,39,40]. Recently, researchers concurred that ATF3 can play both pro-apoptotic and cell survival role depending on the type of stimulation and cell context [21,26,32,36,39].…”

Di‐(2‐ethylhexyl) Phthalate Upregulates ATF3 Expression and Suppresses Apoptosis in Mouse Genital Tubercle

“…For example, ATF3 positively contributed to neuronal survival in stress-induced death 26) , and over-expression of the gene has been shown to confer protection from DNA damageinduced apoptosis 27) . Also, ATF3 inhibited doxorubicininduced apoptosis in cardiac myocytes 28) . DEHP treatment increased ATF3 expression, at ED16.5 with a decrease of apoptosis.…”

Gene Therapy Targets and the Role of Pharmacogenomics in Heart Failure

“…The Activating Transcription Factor (Atf-3), that is also known as a factor protecting the liver, plays a major role in the activation and the regulation of the growth by controlling the expression of genes involved in late response (such as the genes that control the synthesis of the DNA) (Nobori K, 2002). Moreover, the Atf-3 can stop the procedure of apoptosis that may have been initiated as a response to ischemia (Kwaan HC, 2000).…”