http://www.cancer.gov/cancertopics/pdq/cam/prostatesupplements/healthprofessional/page4#Section_76
Modified Citrus Pectin
OverviewGeneral Information and HistoryPreclinical Studies/Animal Studies In vitro studies Animal studiesHuman Studies Intervention studies Current Clinical TrialsAdverse Effects
Overview
This section contains the following key information:
- Citrus pectin is a complex polysaccharide found in the peel and pulp of citrus fruit and can be modified by treatment with high pH and temperature.
- Preclinical research suggests that modified citrus pectin (MCP) may have effects on cancer growth and metastasis through multiple potential mechanisms.
- Very limited clinical research has been done with a couple of citrus pectin-containing products. For prostate cancer patients, the results suggest some potential clinical benefits with relatively minor and infrequent adverse events.
General Information and History
Pectin is a complex polysaccharide contained in the primary
cell
walls of terrestrial plants. The word ‘pectin’ comes from the Greek
word for congealed or curdled. Plant pectin is used in food processing
as a gelling agent and also in the formulation of
oral and
topical medicines as a stabilizer and nonbiodegradable matrix to support controlled
drug delivery.[
1] Citrus pectin is found in the peel and pulp of citrus fruit and can be modified by treatment with high pH and temperature.[
2] Modification results in shorter
molecules that dissolve better in water and are more readily absorbed by the body than are complex, longer chain citrus pectins.[
3] One of the molecular targets of MCP is galectin-3, a
protein
found on the surface and within mammalian cells that is involved in
many cellular processes, including cell adhesion, cell activation and
chemoattraction, cell growth and differentiation, the
cell cycle, and
apoptosis; MCP inhibits galectin-3 activity.[
2]
Some research suggests that MCP may be protective against various types of cancer, including
colon,
lung, and prostate cancer. MCP may exert its anticancer effects by interfering with
tumor cell metastasis or by inducing apoptosis.[
4]
In
a 2007 study, pectins were investigated for their anticancer
properties. Prostate cancer cells were treated with three different
pectins; citrus pectin (CP), Pectasol (PeS, a
dietary supplement
containing modified citrus pectin), and fractionated pectin powder
(FPP). FPP induced apoptosis to a much greater degree than did CP and
PeS. Further analysis revealed that treating prostate cancer cells with
heated CP resulted in levels of apoptosis similar to those following
treatment with FPP. This suggests that specific structural features of
pectin may be responsible for its ability to induce apoptosis in
prostate cancer cells.[
4]
In
a 2010 study, prostate cancer cells were treated with PeS or
PectaSol-C, the only two MCPs previously used in human trials. The
researchers postulated that, because it has a lower molecular weight,
PectaSol-C may have better
bioavailability than PeS. Both types of MCP were tested at a
concentration of 1 mg/mL and both were effective in inhibiting cell growth and inducing apoptosis through inhibition of the MAPK/ERK
signaling pathway and activation of the
enzyme caspase-3.[
6]
In another study, the role of galectin-3, a multifunctional
endogenous lectin, in
cisplatin
-treated prostate cancer cells was examined. Prostate cancer cells that
expressed galectin-3 were found to be resistant to the apoptotic
effects of cisplatin. However, cells that did not express galectin-3
(via silencing
RNA
knockdown of galectin-3 expression or treatment with MCP) were
susceptible to cisplatin-induced apoptosis. These findings suggest that
galectin-3 expression may play a role in prostate cancer cell
chemoresistance and that the
efficacy of cisplatin treatment in prostate cancer may be improved by inhibiting galectin-3.[
7]
Only a few studies have been reported on the effects of MCP in animals bearing
implanted cancers and only one involving prostate cancer.[
8,
9]
The prostate cancer study examined the effects of MCP on the metastasis
of prostate cancer cells injected into rats. In the study, rats were
given 0.0%, 0.01%, 0.1%, or 1.0% MCP (wt/vol) in their drinking water
beginning 4 days after cancer cell injection. The analysis revealed that
treatment with 0.1% and 1.0% MCP resulted in
statistically significant reductions in lung metastases but did not affect
primary tumor growth.[
9]
In a 2007
pilot study, patients with
advanced solid tumors
(various types of cancers were represented, including prostate cancer)
received MCP (5 g MCP powder dissolved in water) 3 times a day for at
least 8 weeks. Following treatment, improvements were reported in some
measures of
quality of life, including physical functioning, global health status,
fatigue, pain, and
insomnia. In addition, 22.5% of participants had
stable disease after 8 weeks of MCP treatment, and 12.3% of participants had disease stabilization lasting more than 24 weeks.[
3]
The effect of MCP on
prostate-specific antigen
(PSA) doubling time (PSADT) was investigated in a 2003 study. Prostate
cancer patients with rising PSA levels received six PeS capsules 3 times
a day (totaling 14.4 g of MCP powder daily) for 12 months. Following
treatment, 7 of 10 patients had a statistically significant (
P ≤ .05) increase in PSADT.[
10]
General information about clinical trials is also available from the
NCI Web site.
In one
prospective pilot study, MCP was well tolerated by the majority of treated patients, with the most commonly reported
side effects being
pruritus,
dyspepsia, and flatulence.[
3]
In another study, no serious side effects from MCP were reported,
although three patients withdrew from the study due to abdominal cramps
and
diarrhea that improved once treatment was halted.[
10]
- Mohnen D: Pectin structure and biosynthesis. Curr Opin Plant Biol 11 (3): 266-77, 2008. [PUBMED Abstract]
- Glinsky
VV, Raz A: Modified citrus pectin anti-metastatic properties: one
bullet, multiple targets. Carbohydr Res 344 (14): 1788-91, 2009. [PUBMED Abstract]
- Azemar
M, Hildenbrand B, Haering B, et al.: Clinical benefit in patients with
advanced solid tumors treated with modified citrus pectin: a prospective
pilot study. Clin Med Oncol 1: 73-80, 2007. Available online
. Last accessed March 20, 2014.
- Jackson
CL, Dreaden TM, Theobald LK, et al.: Pectin induces apoptosis in human
prostate cancer cells: correlation of apoptotic function with pectin
structure. Glycobiology 17 (8): 805-19, 2007. [PUBMED Abstract]
- Ramachandran
C, Wilk BJ, Hotchkiss A, et al.: Activation of human T-helper/inducer
cell, T-cytotoxic cell, B-cell, and natural killer (NK)-cells and
induction of natural killer cell activity against K562 chronic myeloid
leukemia cells with modified citrus pectin. BMC Complement Altern Med
11: 59, 2011. [PUBMED Abstract]
- Yan
J, Katz A: PectaSol-C modified citrus pectin induces apoptosis and
inhibition of proliferation in human and mouse androgen-dependent and-
independent prostate cancer cells. Integr Cancer Ther 9 (2): 197-203,
2010. [PUBMED Abstract]
- Wang
Y, Nangia-Makker P, Balan V, et al.: Calpain activation through
galectin-3 inhibition sensitizes prostate cancer cells to cisplatin
treatment. Cell Death Dis 1: e101, 2010. [PUBMED Abstract]
- Hayashi
A, Gillen AC, Lott JR: Effects of daily oral administration of
quercetin chalcone and modified citrus pectin on implanted colon-25
tumor growth in Balb-c mice. Altern Med Rev 5 (6): 546-52, 2000. [PUBMED Abstract]
- Pienta
KJ, Naik H, Akhtar A, et al.: Inhibition of spontaneous metastasis in a
rat prostate cancer model by oral administration of modified citrus
pectin. J Natl Cancer Inst 87 (5): 348-53, 1995. [PUBMED Abstract]
- Guess
BW, Scholz MC, Strum SB, et al.: Modified citrus pectin (MCP) increases
the prostate-specific antigen doubling time in men with prostate
cancer: a phase II pilot study. Prostate Cancer Prostatic Dis 6 (4):
301-4, 2003. [PUBMED Abstract]
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