Bioactive component, cantharidin from Mylabris cichorii and its antitumor activity against Ehrlich ascites carcinoma

Abstract

The anticancer activity of the extract of blister beetle, Mylabris cichorii has been documented earlier by us. In the present study, the active principle of M. cichorii was isolated and its anticancer efficacy was evaluated against murine Ehrlich ascites carcinoma (EAC). The isolated bioactive compound was characterized to be cantharidin which showed potent antitumor activity and inhibited the proliferation of Ehrlich ascites carcinoma, both in vivo and in vitro. Cantharidin-treated EAC-bearing mice showed about 82% increase in lifespan at the dose of 0.5 mg/kg/day. In vitro cytotoxicity assay with the 3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test revealed about 50% cell death at the concentration of 25.8 μg/ml. The fluorescence and transmission electron microscopy revealed that EAC cells treated with cantharidin depicted typical apoptotic morphology with chromatin condensation, nuclear fragmentation into discrete masses, and plasma membrane blebbing which deduce towards the death of these cells. Histological examination of the kidney of cantharidin-treated mice showed glomerular and tubular congestion with abnormal Bowman's capsule, thus, indicating a renal toxicity in the host. Cantharidin-induced renal damage in the host was also manifested by the decreased lactate dehydrogenase isozymes and its possible release from the cells.

Clinical Study on Safety of Cantharidin Sodium and Shenmai Injection Combined with Chemotherapy in Treating Patients with Breast Cancer Postoperatively

“…Cantharidin is a sesquiterpene derivatives extracted from the Mylabris body (Verma et al, 2012 DOI:http://dx.doi.org/10.7314/APJCP.2014.15.14.5597 …”

Cantharidin Combined with Chemotherapy for Chinese Patients with Metastatic Colorectal Cancer

“…Cantharidin is a sesquiterpene derivatives extracted from the Mylabris body (Verma et al, 2012). Cantharidin sodium is a semi-synthetic derivative of cantharidin.…”

8-60hIPP5m-Induced G2/M Cell Cycle Arrest Involves Activation of ATM/p53/p21cip1/waf1Pathways and Delayed Cyclin B1 Nuclear Translocation

“…Neutralizing PP1 by anti-PP1 antibodies, mutation of PP1, or treatment with various natural phosphatase inhibitors such as okadaic acid, calyculin-A, tautomycin, microcystin-LR, fostriecin and cantharidin have been shown to cause abnormalities in cell cycle progression and checkpoint abrogation (Axton et al, 1990;Kinoshita et al, 1990;Edelson et al, 2011;Honkanen et al, 2012;Rubiolo et al, 2012). In particular, fostriecin and cantharidin have been shown to force cells to go through the cycle prematurely and into mitosis, resulting in multiple aberrant mitotic spindles and apoptotic cell death (Verma et al, 2012;Theobald et al, 2013). In human cells, PP1 could act as a histone H1 phosphatase, which is required for chromatin decondensation during the exit from mitosis (Paulson et al, 1996).…”