Rugosin E, an ellagitannin, inhibits MDA-MB-231 human breast cancer cell proliferation and induces apoptosis by inhibiting nuclear factor-κB signaling pathway

External Qi of Yan Xin Qigong Induces Apoptosis and Inhibits Migration and Invasion of Estrogen-Independent Breast Cancer Cells Through Suppression of Akt/NF-ĸB Signaling

“…Akt and NF-κB are constitutively activated in MDA-MB-231 cells [14,16]. In the present study we show that YXQ-EQ induced apoptosis and inhibited migration and invasion of MDA-MB-231 cells through suppression of Akt/NF-κB signaling.…”

“…NF-κB has been reported to regulate the expression of many genes that are associated with tumor development, including antiapoptotic, pro-invasion, and cell cycle-regulatory genes [12][13][14][15]. NF-κB inactivation has been reported to induce growth inhibition and apoptosis in breast cancer cells or sensitize breast cancer cells to apoptosis [16][17][18][19]. The inhibition of Akt has been shown to repress growth and invasive capacity of breast cancer cells [20].…”

Anti-hyperplasia effects of Rosa rugosa polyphenols in rats with hyperplasia of mammary gland

“…Reports show that R. rugosa contains high amount of polyphenols including catechin, kaempferol, quercetin, apigenin, gallic acid and so on (Lee et al, 2008;Zhang et al, 2014). The polyphenols derived from R. rugosa can inhibit the proliferation of MDA-MB-231 mammary cells through mediating NFB-p65 signaling pathway (Kuo et al, 2007). These are inline with the phenomena in our present study.…”

“…NFB is an important transcriptional factor in the regulation of inflammatory, immune and apoptotic responses. NFB can be activated by a variety of external stimuli and subsequently stimulates several proinflammatory cytokines and anti-apoptotic genes expressions (such as COX-2 and VEGF) Kim et al, 2012;Kuo et al, 2007). Activations of the classical MAPK pathway and AKT pathway are early premalignant phenomena.…”

Increased H2O2 level in exhaled breath condensate in primary breast cancer patients

“…That mechanistically provides an example of the intersection between inXammatory and cell cycle regulators. In human breast cancer cells TNF stimulates both constitutive and inducible NF-B resulting in increased expression of cyclin D1 and c-Myc (Kuo et al 2006). There is a considerable crosstalk among the various pathways and between stromal and epithelial cells driving the proliferation of normal and malignant breast epithelial cells.…”