Abstract 2246: Anti-proliferative activities of lipid fraction of extract from the skin of the catfish Arius Bilineatus, Valenciennes

• Published in: Cancer research (Chicago, Ill.) Ill.), 2017-07, Vol.77 (13_Supplement), p.2246-2246
• Main Authors: Yang, Peiying, Ding, Jibin, Pan, Yong, Jiang, Yan, Afzal, Mohammad, Paul, Bincy M., George, Sosamma O., Al-Hassan, Jassim M.
• Format: Article
• Language: English
• ISSN: 0008-5472; 1538-7445
• DOI: 10.1158/1538-7445.AM2017-2246

The catfish (Arius bilineatus, Val.) secretes a gelatinous substance composed of biochemically active lipids and proteins from its skin upon stress or injury. Preparations from the skin have previously been shown to affect blood clotting and accelerates healing of non-healing diabetic foot ulcers in man. We have reported previously fish skin preparation (CSP) derived from the skin of the Catfish and it’s lipid fraction exerted anti-inflammatory activity in the in vitro cells and in vivo animal models. Here anti-proliferative effect of a lipid fraction of fish skin preparation (CSP-L) derived from the skin of the catfish and its plausible mechanism were investigated in human hepatocellular carcinoma (HCC) Hep3B and human pancreatic cancer Panc-1 cells. Cells were treated with CSP-L (0 to 100 μg/ml) for 72 hrs and cell proliferation was measured by the MTT assay. The results showed much stronger inhibition by CSP-L in Panc-1 cells than that of Hep3B cells with IC50 of 5.5 ± 1.4 μg/ml and 19.5 ± 7.7 μg/ml, respectively. Cell cycle analysis with PI staining suggested that CSP-L (25 - 100 μg/ml) led to G1 phase arrest in Hep3B cells whereas S phase arrest was observed in Panc-1 cells, suggesting the differential molecular mechanisms responsible for CSP-L induced cell growth suppression in Hep3B and Panc-1 cells. The alteration of cell cycle was concentration dependent. Additionally, CSP-L concentration dependently suppressed the invasion of Hep3B and Panc-1 cells. The molecular mechanism associated with CSP-L’s anti-proliferative effect was examined by Western blotting in both Hep3B and Panc-1 cells. Intriguingly, CSP-L (50 and 100 μg/ml) notably decreased protein levels of cyclin D, Stat3, pRB and pERk in Hep3 B cells in a concentration dependent manner. In contrast, only pRB and pERK protein expression were reduced in CSP-L treated Panc-1 cells. These again suggest that CSP-L inhibited the proliferation of Hep3B and Panc-1 cells by different molecular mechanisms. Collectively, our preliminary data suggest that CSP-L has a great potential to be developed as an anticancer or preventive agent for both HCC or pancreatic cancer and warrants further investigation. This study was support by a grant from Kuwait Foundation for the Advancement of Science No. KFAS 2013-120701A-D, and Kuwait University Research Grant No. SL03/14. Citation Format: Peiying Yang, Jibin Ding, Yong Pan, Yan Jiang, Mohammad Afzal, Bincy M. Paul, Sosamma O. George, Jassim M. Al-Hassan. Anti-pro