2013
DOI: 10.1016/j.biopha.2013.05.001
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Anti-tumor effect of 4-Amino-2-Trifluoromethyl-Phenyl Retinate on human breast cancer MCF-7 cells via up-regulation of retinoid receptor-induced gene-1

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Cited by 19 publications
(11 citation statements)
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“…In the present study, ATPR inhibited gastric cancer cell growth to a greater extent compared with ATRA. The anti-proliferative effects of ATPR are consistent with those reported in previous in vivo and in vitro studies (24). ATPR reduced the cyclin E level in MKN-74 cells, and altered cell cycle progression in the AGS and MKN-74 cells; however, no such effects were observed following treatment with ATRA.…”
Section: Discussionsupporting
confidence: 90%
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“…In the present study, ATPR inhibited gastric cancer cell growth to a greater extent compared with ATRA. The anti-proliferative effects of ATPR are consistent with those reported in previous in vivo and in vitro studies (24). ATPR reduced the cyclin E level in MKN-74 cells, and altered cell cycle progression in the AGS and MKN-74 cells; however, no such effects were observed following treatment with ATRA.…”
Section: Discussionsupporting
confidence: 90%
“…In addition to influencing cell growth and apoptosis, RA analogs, including ATPR, can induce cell differentiation in embryonic and adult tissues (1,2,24). Similarly, RA and a number of its analogs inhibit tumor progression by inducing cell differentiation (16), possibly through phosphatidylinositol 3-kinase (PI3K) signaling (35).…”
Section: Discussionmentioning
confidence: 99%
“…Several researches indicated that ATRA was able to induce morphological differentiation and control cells invasion and migration of many types of tumors (Garattini et al, 2014;Hu et al, 2014b;Zhang et al, 2014a), making it the foremost inducing differentiation therapeutic agent. However, because of its instability and toxicity (Gui et al, 2011;Wang et al, 2013c), ATRA was not applied extensively in clinical except for dermatosis. In the study of our lab, ATPR, a novel derivative of ATRA, with the advantage of lower toxicity and better stability, showed more intense pharmacological action on biological behavior of A549 cells.…”
Section: Discussionmentioning
confidence: 99%
“…In our previous studies, it was explored that ATPR might inhibit tumor cells migration by down-regulating the expression of MLCK involving p38 signaling pathway (Wang et al, 2013a), one of MAPKs pathway cascade. The mitogen-activated protein kinases (MAPKs) cascades include three classical signal pathways: p38, ERK1/2 and JNK, which play crucial roles in different physiological processes, such as cell growth, apoptosis and inflammatory reaction (Zhu et al, 2012b;2014a;Wang et al, 2013c). It was also reported that the elevation of ERK1/2 might activate the MLCK along with a series of downstream pathways activation (Srinivas et al, 2004;Zhou et al, 2008;Muralidharan-Chari et al, 2009;Zhu et al, 2012b;2014a;Harrison et al, 2013).…”
Section: Introductionmentioning
confidence: 99%
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