Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways

Abstract

Abstract. Esophageal cancer is the most common gastrointestinal cancer. Psoralidin exhibits antioxidant, anti-apoptotic, anti-inflammatory and antitumor effects, which result in the inhibition of cancer formation. The present study aimed to investigate the effect of psoralidin on esophageal carcinoma proliferation and growth, and to elucidate its underlying mechanism of action. The effect of psoralidin on cell proliferation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium brom ide assay. Using a n a n nexin V-f luorescein isothiocyanate/propidium iodide apoptosis detection kit and 4' ,6-diamidino-2-phenylindole staining assay, the present study demonstrated that psoralidin significantly enhanced apoptosis of human esophageal carcinoma Eca9706 cells. In addition, caspase-3 activity was analyzed with a caspase-3 colorimetric assay kit, while nuclear factor (NF)-κB activity and protein phosphatidylinositol 3-kinase (PI3K)/Akt expression were measured with an NF-κB enzyme-linked immunosorbent assay kit and western blot analysis, respectively. Eca9706 cells were treated with a PI3K agonist in order to investigate the mechanism of action of psoralidin. It was observed that psoralidin was able to decrease the proliferation and promote the cellular apoptosis of Eca9706 cells in a dose-dependent manner. Furthermore, psoralidin was also able to inhibit the caspase-3 activity of Eca9706 cells in a dose-dependent manner. In addition, psoralidin inhibited NF-κB activity and reduced PI3K and Akt protein expression in Eca9706 cells. Notably, the PI3K agonist was able to reverse the effect of psoralidin on Eca9706 cells. The results of the present study demonstrated that psoralidin was able to inhibit proliferation and enhance apoptosis of human esophageal carcinoma cells via the NF-κB and PI3K/Akt signaling pathways.

Psoralidin prevents caffeine-induced damage and abnormal differentiation of bone marrow mesenchymal stem cells via the classical estrogen receptor pathway

“…Therefore, we aimed to investigate whether PL could reverse excessive caffeine-caused injury in vitro and in vivo and, if so, to elucidate the underlying mechanisms. Documented studies have demonstrated that PL regulates several extracellular signaling pathways, which include the protein kinase B/glycogen synthase kinase 3β/β-catenin signaling pathway, the nuclear factor-kappa B (NF-κB) and phosphatidylinositol 3 kinase (PI3K)/Akt signaling pathway, and the NF-κB and B-cell lymphoma-2 (Bcl-2)/ Bcl-2 associated X protein (Bax) signaling pathway (16,29,30). Previous studies have demonstrated that PL can inhibit the formation of adipocytes by modulating the classical and membrane ER pathways (16).…”

Pharmacological Activities of Psoralidin: A Comprehensive Review of the Molecular Mechanisms of Action

“…PSO promotes cellular apoptosis and inhibits the cancer cells proliferation in prostate cancer (Szliszka et al, 2011;Das et al, 2014); breast cancer (Dwarampudi et al, 2012); liver cancer (Luo et al, 2013); colon cancer (Jin et al, 2016a); esophagal carcinoma (Jin et al, 2016b), or modulate the autophagy in the lung (Hao et al, 2014;Xin et al, 2019).…”

“…PSO significantly decreases cell proliferation and promotes apoptosis of Eca9706 cells in a dose-dependent manner. Moreover, it suppresses caspase-3 and NF-κB activities and also decreases the phosphatidylinositol-3-kinase (PI3K) and protein kinase B (Akt) protein expression dose-dependently (Jin et al, 2016b). Other in vitro studies on cell lines reported that PSO binds to both types of alpha and beta estrogen receptors, activating the classic estrogen receptor signaling pathway, thus explaining the effect of reducing bone loss as well as the antioxidant action (Liu et al, 2014).…”

Development of an UPLC–MS/MS assay to determine psoralidin in rat plasma and its application in a pharmacokinetic study after intragastric administration

“…Psoralidin can also induce cells to produce reactive oxygen species (ROS), thereby inducing DNA damage and autophagy in breast cancer MCF-7 cells [18]. Jin et al [19] demonstrates that psoralidin can inhibit the proliferation and enhance apoptosis of human esophageal cancer cells by affecting NF-0202B and PI3K/Akt signaling pathways. Wang's study indicates that psoralidin has antioxidant activity and α-glucosidase inhibitory activity [20].…”