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FTIR microspectroscopic analysis of sodium butyrate induced differentiation in colon cancer cells in a time‐dependent manner
Author(s) -
Ozek Nihal Simsek,
Gok Seher,
Banerjee Sreeparna,
Severcan Feride
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1006.4
Subject(s) - butyrate , sodium butyrate , chemistry , butyric acid , lipid droplet , cellular differentiation , biochemistry , cancer cell , lauric acid , cell , apoptosis , fatty acid , cancer , fermentation , biology , genetics , gene
Butyric acid is a product of dietary fiber fermentation in the colon. Previous studies showed that this fatty acid inhibited cell proliferation and caused cell differentiation and apoptosis. It has been known that there is a relation between the tumorigenesis of colon cancer and the poor differentiation of colonic epithelial cells. Although the effects of butyrate on cellular differentiation has been documented at molecular level, the butyrate‐induced changes in the content of cancer cell macromolecules such as saturated, unsaturated lipids, protein and glycogen are less understood. The objective of this study was to clarify these changes in colon cancer cells in a time dependent manner using Fourier Transform Infrared (FTIR) microscopy. In this study, CaCo‐2 cells were treated with 3mM sodium butyrate (NaB) and cultured for 12, 24 and 48h. The macromolecular structural and function alterations induced by NaB were determined from spectral analysis of chemical maps of the studied groups. An increase in saturated and unsaturated lipid and a decrease in the triglyceride, and protein content has been obtained in 48 h treated group with respect to the other groups. The variation in membrane fluidity and lipid order has been also determined for this treated group. This study demonstrated that FTIR imaging enables to determine the colon cancer differentiation at the cellular level. This work is supported by METU‐BAP 07.02.2012.004 .

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