Linoleic acid suppresses colorectal cancer cell growth by inducing oxidant stress and mitochondrial dysfunction
Lu X, Yu H, Ma Q, Shen S, Das UN
Lipids in health and disease · 111 citations
Review labels
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How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
Based on full-text disclosure statement.
Publication
- Published
- 2010-09-24 · Lipids Health Dis · vol. 9 · issue 1 · p. 106
- Publisher
- BioMed Central
- Cited
- 155 citations · more than 85% of similar papers · 1.7× the field average
- References
- 25 works
- Access
- Open access (journal) · CC-BY
- Research areas
- Cancer, Lipids, and Metabolism · Eicosanoids and Hypertension Pharmacology · Fatty Acid Research and Health
- Keywords
- Apoptosis, Oxidative stress, Mitochondrial ROS, Reactive oxygen species, Cancer cell, Cell growth, Mitochondrion, Malondialdehyde, Cell culture, Biology, Cytotoxic T cell, Superoxide dismutase, Chemistry, Cancer research, Molecular biology, Biochemistry, Cancer, In vitro
- MeSH
- cell line, tumor, humans, colorectal neoplasms, mitochondrial diseases, reactive oxygen species, malondialdehyde, superoxide dismutase, linoleic acid, apoptosis, cell differentiation, cell proliferation, oxidative stress, osmolar concentration, caspase 3, membrane potential, mitochondrial
5 authors
From CN, IN
- Xiaofeng LuZhejiang A & F University; Zhejiang University
- Haining YuZhejiang University of Technology
- Qi MaZhejiang University
- Shengrong Shen · correspondingZhejiang University
- Undurti Narasimha Das · correspondingJawaharlal Nehru Technological University, Kakinada; Krishna Institute of Medical Sciences
Abstract
Some polyunsaturated fatty acids (PUFAs), if not all, have been shown to have tumoricidal action, but their exact mechanism(s) of action is not clear. In the present study, we observed that n-6 PUFA linoleic acid (LA) inhibited tumor cell growth at high concentrations (above 300 μM); while low concentrations (100-200 μM) promoted proliferation. Analysis of cell mitochondrial membrane potential, reactive oxygen species (ROS) formation, malondialdehyde (MDA) accumulation and superoxide dismutase (SOD) activity suggested that anti-cancer action of LA is due to enhanced ROS generation and decreased cell anti-oxidant capacity that resulted in mitochondrial damage. Of the three cell lines tested, semi-differentiated colorectal cancer cells RKO were most sensitive to the cytotoxic action of LA, followed by undifferentiated colorectal cancer cell line (LOVO) while the normal human umbilical vein endothelial cells (HUVEC) were the most resistant (the degree of sensitivity to LA is as follows: RKO > LOVO > HUVEC). LA induced cell death was primed by mitochondrial apoptotic pathway. Pre-incubation of cancer cells with 100 μM LA for 24 hr enhanced sensitivity of differentiated and semi-differentiated cells to the subsequent exposure to LA. The relative resistance of LOVO cells to the cytotoxic action of LA is due to a reduction in the activation of caspase-3. Thus, LA induced cancer cell apoptosis by enhancing cellular oxidant status and inducing mitochondrial dysfunction.
Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).
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