Molecular mechanisms of the action of Arctigenin in cancer

Abstract

Since antediluvian times, the scientific community has realized that natural compounds exhibit enormous potential for the treatment of terrible diseases, such as cancer. Despite a variety of effective bioactive molecules, effective therapies still need to be developed to treat cancer. Hence, it is necessary to study the interactions of natural molecules with their cellular targets. Arctigenin (ATG), a natural lignan compound extracted from Arctium lappa, inhibits the growth of various cancer cells, such as those of the stomach, lungs, liver, and colon, as well as leukocytes, and regulates numerous intracellular activities, such as antioxidative, anti-inflammatory, and anticancer activities. The intention of this paper is to summarize and generally analyse the molecular pathways that are involved in the anticancer effects of ATG. In addition, the interactions of ATG with other drugs are also highlighted in this paper.

Targeting Foam Cell Formation in Atherosclerosis: Therapeutic Potential of Natural Products

“…Arctigenin. Arctigenin, a phenylpropanoid dibenzylbutyrolactone lignin, has many beneficial biologic effects, such as immune modulation and regulation of metabolic disorders (Huang et al, 2012a;He et al, 2018). In oxLDL-loaded THP-1 macrophages, the expression of ApoE, ABCA1, and ABCG1 were increased by arctigenin (50 and 100 mM), resulting in promoting cholesterol efflux (Xu et al, 2013d).…”

Arctigenin Attenuates Breast Cancer Progression through Decreasing GM-CSF/TSLP/STAT3/β-Catenin Signaling

“…Arctigenin has been reported to possess several pharmacological activities, including anti-oxidant, anti-inflammatory and anti-tumor [17][18][19]. In several types of tumor, arctigenin has been reported to exert anti-tumor effects via inhibiting the nuclear translocation of NF-κB [20]. In breast cancer, arctigenin induces apoptosis of breast cancer cells and confers anti-metastatic effects [21][22][23].…”

ERN1 knockdown modifies the effect of glucose deprivation on homeobox gene expressions in U87 glioma cells

“…This is important for the evaluation of possible significance of in ERN1 dependent control of glioma cell proliferation because endoplasmic reticulum stress signaling mediated by ERN1 is involved in numerous metabolic pathways and ERN1 knockdown has clear anti-tumor effects (Auf et al 2010(Auf et al , 2013Bravo et al 2013;Manie et al 2014;Minchenko et al 2014Minchenko et al , 2015aLogue et al 2018). Furthermore, there are data that glucose deprivation can enhance the sensitivity of cancer cells to anti-cancer drugs, particularly arctigenin, which inhibits the growth of various cancer cells and induces tumor cell death under glucose deprivation condition possibly by blocking the unfolded protein response and by inhibiting cellular energy metabolism (Awale et al 2006;Kim et al 2010;Gu et al 2012;He et al 2018). Results of our study clarify possible mechanisms of glucose deprivation on the proliferation/surviving of ERN1 knockdown glioma cells through specific changes in the expression of genes encoding important homeobox proteins.…”

“…Furthermore, there are data indicating that glucose is an important factor for cancer cells chemoresistance (Awale et al 2006). Thus, arctigenin, a natural lignan compound extracted from Arctium lappa, inhibits the growth of various cancer cells and induces tumor cell death under glucose deprivation possibly by blocking the unfolded protein response (Awale et al 2006;Kim et al 2010;Gu et al 2012;He et al 2018). Moreover, this antitumor agent has ability to eliminate the tolerance of cancer cells to glucose deprivation, but glucose deprivation leads to suppression of chemoresistance through unknown mechanisms.…”