Sanguinarine overcomes P-glycoprotein-mediated multidrug-resistance via induction of apoptosis and oncosis in CEM-VLB 1000 cells

Sanguinarine-Induced Apoptosis in Human Leukemia U937 Cells via Bcl-2 Downregulation and Caspase-3 Activation

“…Recently, several studies have reported that treatment with sanguinarine caused the accumulation of cells in the G1 phase of the cell cycle and apoptosis, which suggests that the growth-inhibitory effect of sanguinarine is the result of a G1 phase block, and that such cells do not enter the S phase [11][12][13][14][15][16][17] . While the cell killing mechanism of sanguinarine has been investigated, little is known about the effects of this compound on the growth of cancer cells.…”

“…This compound is a structural homologue of chelerythrine, and has been shown to possess antimicrobial, antioxidant, and anti-inflammatory properties [7][8][9] . Several studies have indicated that sanguinarine, at micromolar concentration, inhibits the growth of various human cancer cell lines that are associated with cell cycle arrest and stimulation of apoptotic cell death [10][11][12][13][14][15][16][17] . However, the underlying mechanisms of its action in leukemia are not completely understood.…”

Alkaloids from Toddalia asiatica and their cytotoxic, antimicrobial and antifungal activities

“…They have also been reported to be a NFjB (nuclear transcription factor jB) inhibitor (Gopalakrishna, Chen, & Gundimeda, 1995), a DNA intercalator (binding to guanosine-cytosine rich regions) (Weerasinghe, Hallock, Tang, Trump, & Liepins, 2006), a RNA intercalator (binding to specific poly(A) tail of mRNA) (Giri & Kumar, 2008;Islam et al, 2007), a topoisomerase I and II inhibitor (Fang, Wang, & Hecht, 1993), an inhibitor of tubulin assembly (Wolff & Knipling, 1993), an inhibitor of Na + /K + ATPase (Giri & Kumar, 2008) and a generator of DNA adducts (Weerasinghe et al, 2006). Additionally, it was reported that Benzo[c]phenanthridine alkaloids modulated the function of various enzymes, such as mitogen-activated protein kinase phosphatase-1, protein kinase C (Gopalakrishna et al, 1995), phosphoinositide-dependent protein kinase 1 (Vrba et al, 2009), and inhibited Mitogen-activated protein kinase phosphatase-1 (MKP-1) (Vogt et al, 2005).…”

A new method to induce multi-drug resistance to carboplatin in a mouse model of human tongue squamous cell carcinoma

“…GST-p detoxifies xenobiotics such as CBP 6,7,12,16 , and is known to be over-expressed in tumors compared with normal tissues. MRP 1 , GST-p and Topo II over-expression has been correlated with the development of many types of cancers in vitro 2,3,5,6,12,18,19 and in vivo 3,16 . Inhibition of these proteins has been shown to inhibit the growth of various carcinomas 14,17,21 .…”