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Seher A Khan, Department of Pharmaceutical Sciences, Lake Erie College of Osteopathic Medicine School of Pharmacy, Erie, PA 16509, United States Correspondence to: Seher A Khan, PhD, Department of Pharmaceutical Sciences, Lake Erie College of Osteopathic Medicine School of Pharmacy, Erie, PA 16509, United States. seherkhan@lecom.edu Telephone: +1-814-8605169 Fax: +1-814-8668450 Received: 2006-12-19 Accepted: 2007-02-01
© 2007 The WJG Press. All rights reserved.
Key words: Colon cancer; Fatty acid; Receptor
Khan SA. Bitter gourd (Momordica charantia): A potential mechanism in anti-carcinogenesis of colon. World J Gastroenterol 2007; 13(11): 1761-1762
http://www.wjgnet.com/1007-9327/13/1761.asp
TO THE EDITOR Bitter gourd (Momordica charantia), has received widespread attention in the scientific community due to its beneficial effects, including anti-diabetic, anti-cancer and anti-inflammatory effects in laboratory studies[1]. However, a well-defined mechanism by which this important plant food exerts its beneficial effects has not been elucidated. We present some of the latest findings on the plant’s effects against colon cancer.
Bitter
gourd seeds are enriched with 9c 11t 13t (9 cis, 11 trans,
13 trans) conjugated linolenic acid (CLN)[2]. CLN
collectively refers to a group of linolenic acid (18:3; c9, c11, c13)
derivatives with positional (double bonds in carbon 9, 11 and 13 or 8,
10 and 12) and geometric (cis, Z and trans, E) isomers.
Interestingly, 9c 11t 13t CLN-enriched bitter gourd seed extracts
protect colon from chemical-induced carcinogenesis in rats[3].
The fatty acid significantly reduced the incidences as well as
multiplicity of colonic adenocarcinoma. In a separate, short-term study,
bitter gourd seed oil significantly reduced the number and frequency of
aberrant crypt foci (ACF) in the colon of male F-344 rats treated with
azoxymethane[4]. In an attempt to elucidate a possible receptor-mediated mechanism of anti-carcinogenesis, bitter gourd seed oil has been shown to increase the expression of peroxisome proliferator-activated receptor gamma (PPARg), a member of nuclear hormone receptor superfamily[7]. Furthermore, 9c 11t 13t CLN activated PPARg in transfection experiments[8], its effect comparable to BRL-49653, a specific ligand for PPARg. These important studies indicate that bitter gourd’s effect in the colon may be mediated in part by PPARg. Functionally, PPAR is a ligand-activated transcription factor, which is involved in gene expression in a tissue-, sex- and species-dependent manner. Upon activation, PPAR forms a heterodimer with RXRa and regulates gene expression by binding to PPAR-response elements (PPRE) on responsive genes. Target genes for PPAR include lipid metabolizing enzymes and growth regulatory genes. To date, three subtypes of PPAR (a, b and g) have been identified in several species including human[9]. PPARg is highly expressed in normal human colon and colon tumors as well as cell lines derived from colon cancer[10]. Expression of this receptor subtype in colon cells has been found equal to or even greater than adipose tissue, where it was originally characterized[10]. PPARg activation has been shown to inhibit cell growth, promote differentiation and stabilize genes that are altered in colon cancer[10-12]. The current prevailing belief is that PPARg's ability to enhance differentiation and apoptosis is a positive event, associated with cell-cycle arrest and reduced proliferation[12]. Similar beneficial effects (growth inhibition, induction of apoptosis) were observed with bitter gourd against colon carcinogenesis[3-7]. Taken together, there is an association of PPARg in CLN-mediated effects in the colon. Further studies are required to understand the detailed mechanism.
REFERENCES
1
Grover JK, Yadav SP. Pharmacological actions and potential uses
of Momordica charantia: a review. J Ethnopharmacol
2
Takagi T, Itabashi Y. Occurrence of mixtures of geometrical
isomers of conjugated octadecatrienoic acid in some seed
3
Kohno H, Yasui Y, Suzuki R, Hosokawa M, Miyashita K, Tanaka T.
Dietary seed oil rich in conjugated linolenic acid from
4
Kohno H, Suzuki R, Noguchi R, Hosokawa M, Miyashita K, Tanaka T.
Dietary conjugated linolenic acid inhibits
5
Tsuzuki T, Tokuyama Y, Igarashi M, Miyazawa T. Tumor growth
suppression by alpha-eleostearic acid, a linolenic acid
6
Yasui Y, Hosokawa M, Kohno H, Tanaka T, Miyashita K. Troglitazone
and 9cis, 11 trans, 13 trans-conjugated linolenic
7
Yasui Y, Hosokawa M, Sahara T, Suzuki R, Ohgiya S, Kohno H,
Tanaka T, Miyashita K. Bitter gourd seed fatty acid rich
8
Chao CY, Huang CJ. Bitter gourd (Momordica charantia) extract
activates peroxisome proliferator-activated receptors
9
Lemberger T, Braissant O, Juge-Aubry C, Keller H, Saladin R,
Staels B, Auwerx J, Burger AG, Meier CA, Wahli W. PPAR
10
Sarraf P, Mueller E, Jones D, King FJ, DeAngelo DJ, Partridge JB,
Holden SA, Chen LB, Singer S, Fletcher C, Spiegelman
11
Brockman JA, Gupta RA, Dubois RN. Activation of PPARgamma leads
to inhibition of anchorage-independent growth of
12
Kitamura S, Miyazaki Y, Shinomura Y, Kondo S, Kanayama S,
Matsuzawa Y. Peroxisome proliferator-activated receptor
S- Editor Liu Y L- Editor Zhu LH E- Editor Che YB
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