rhamnogalacturonan-i and Colonic-Neoplasms

To examine the anti-metastatic activities of polysaccharides in broccoli, purified polysaccharides (BCE-I, -II, and -III) were isolated by fractionation of broccoli enzyme extracts and subsequent ethanol precipitation. BCE-I mainly consisted of galactose and arabinose, whereas BCE-II mainly consisted of galacturonic acid and rhamnose, and BCE-III mainly consisted of rhamnose and galactose. Of the three fractions, stimulation of murine peritoneal macrophages by BCE-I showed the greatest enhancement of tumor necrosis factor-α, interleukin (IL)-12, and IL-6 secretion. In addition, intravenous (i.v.) administration of BCE-I enhanced the lethal activity of natural killer (NK) cells on YAC-1 tumor cells significantly and dose-dependently in an

Topics: Animals; Antineoplastic Agents, Phytogenic; Brassica; Colonic Neoplasms; Female; Humans; Immunity, Innate; Interleukin-12; Interleukin-6; Killer Cells, Natural; Lung Neoplasms; Macrophage Activation; Macrophages, Peritoneal; Mice; Mice, Inbred BALB C; Neoplasm Metastasis; Pectins; Plant Extracts; Polysaccharides

Pectin modified with pH, heat or enzymes, has previously been shown to exhibit anti-cancer activity. However, the structural requirements for modified pectin bioactivity have rarely been addressed. In this study several pectin extracts representing different structural components of pectin were assessed for effects against colon cancer cells. Rhamnogalacturonan I (RGI) extracts reduced proliferation of DLD1 and HCT116 colon cancer cells in a dose- and time-dependent manner. RGI reduced ICAM1 gene expression and siRNA-mediated knockdown of ICAM1 expression decreased cell proliferation providing a potential novel mechanism for the anti-cancer activity of pectin. Structural analysis of bioactive and non-bioactive RGIs suggested that a homogalacturonan component is maybe essential for the anti-proliferative activity, furthering the understanding of the structural requirements for pectin bioactivity.

Topics: Antineoplastic Agents; Cell Line, Tumor; Cell Proliferation; Colonic Neoplasms; HCT116 Cells; Humans; Intercellular Adhesion Molecule-1; Magnetic Resonance Spectroscopy; Pectins; RNA Interference; RNA, Small Interfering

Pectin is an important dietary component of all fruits and vegetables. Some pectins have been shown to inhibit cancer cell growth, but the effective structures and mechanisms have remained unclear. In this study, we investigated the effects of four structurally distinct pectins on human colon cancer HT-29 cells and the possible mechanisms accounting for the actions. The proliferation inhibitory effect was examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Flow cytometry was used to visualize the cell cycle distribution. An reverse transcription polymerase chain reaction (RT-PCR)-based assay was utilized to detect mRNA levels of the proteins related to cell cycle arrest. The data showed that the rhamnogalacturonan I domain-rich pectin from potato inhibited the proliferation of HT-29 cells and induced significant G2/M cell cycle arrest. This inhibitory effect was due to the down-regulation of cyclin B1 and cyclin-dependent kinase 1 expression, but not p21(WAF1/CIP1) expression. The results suggested that the rhamnogalacturonan I domain might relate to the anticancer activity of pectin.

Topics: Antineoplastic Agents, Phytogenic; Cell Cycle Checkpoints; Cell Cycle Proteins; Cell Proliferation; Colon; Colonic Neoplasms; Down-Regulation; HT29 Cells; Humans; Pectins; Phytotherapy; Plant Preparations; RNA, Messenger; Solanum tuberosum