N-3 PUFAs have antiproliferative and apoptotic effects on human colorectal cancer stem-like cells in vitro

Yang, Ting; Shi, Fang; Zhang, Haixia; Xu, Lixiao; Zhang, Zhanqiang; Yuan, Kaitao; Xue, Conglong; Yu, Honglan; Zhang, Sheng; Li, Yufei; Hanping, Shi; Zhang, Yan

doi:10.1016/j.jnutbio.2012.03.023

Cited by 65 publications

(49 citation statements)

References 38 publications

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“…The impact of HFD on the development of liver fibrosis and HCC formation may be related to the inhibitory effect of HFD on cell proliferation and induction of apoptosis [15,39]. In vitro studies have shown that cholesterol deficiency in the culture medium could promote the neoplastic cellular growth [40,41].…”

Section: Discussionmentioning

confidence: 99%

High-saturate-fat diet delays initiation of diethylnitrosamine-induced hepatocellular carcinoma

et al. 2014

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BackgroundNonalcoholic fatty liver disease (NAFLD) is a risk factor for hepatocellular carcinoma (HCC), but the association between a high-fat diet (HFD) and HCC is not fully understood. In this study, we investigated whether a high-saturate-fat diet affects hepatocarcinogenesis induced by administration of diethylnitrosamine (DEN).MethodsAdult SD rats were randomized into the following groups: normal chow diet (NCD), HFD, NCD + DEN, and HFD + DEN. The HFD contains 2% cholesterol and 10% lard oil. In mice with DEN treatment, the carcinogen was given via gavage. Mice were sacrificed at the end of 10, 12, and 14 weeks, respectively. The effects of HFD on hepatic carcinogenesis were assessed by HCC incidence, tumor differentiation, and the number and size of tumor nodules. Western blot and immunohistochemistry for proliferating cell nuclear antigen (PCNA), enzyme-linked immunosorbent assay (ELISA) for caspase-3, and real-time PCR for TNF-α and IL-6 further uncovered the proliferative and apoptotic properties of liver.ResultsIn contrast to the NCD group, DEN treatment (NCD + DEN group) led to hepatitis, cirrhosis, hepatic tumor, and decreased body weight. Interestingly, HFD, which induced hyperlipidemia and hepatic steatosis, attenuated DEN-related malnutrition and fibrosis progression in HFD + DEN group during 10–14 weeks. Moreover, the HFD + DEN group exhibited that the proportion of well differentiated HCC was much higher than that of NCD + DEN group. The number and average volume of HCC node were also significantly lowered in HFD + DEN group (P < 0.01-0.05). When compared to that of NCD + DEN group, there was an inhibited expression of PCNA, TNF-α, and IL-6, and activation of caspase-3 in the liver of HFD + DEN group at week 10 and 12.ConclusionsHFD restores malnutrition in the DEN-treated rats, which in turn inhibits the initiation of hepatic carcinogenesis and malignancy.

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Section: Discussionmentioning

confidence: 99%

High-saturate-fat diet delays initiation of diethylnitrosamine-induced hepatocellular carcinoma

et al. 2014

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“…Defects in the apoptotic pathway are widely observed in cancer cells. The pro-apoptotic effect of DHA on cancer cells has been widely documented both in vitro and in vivo in various types of cancer cells such as colon HT-29 [45], gastric AGS [46], pancreatic Paca-44 [47], lung 549 [48], and colorectal stem-like [49] cancer cells. …”

Section: Dha Induces Apoptotic Signaling and Affects Dna Damage Rementioning

confidence: 99%

Docosahexaenoic Acid Induces Oxidative DNA Damage and Apoptosis, and Enhances the Chemosensitivity of Cancer Cells

Song

Kim

2016

IJMS

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The human diet contains low amounts of ω-3 polyunsaturated fatty acids (PUFAs) and high amounts of ω-6 PUFAs, which has been reported to contribute to the incidence of cancer. Epidemiological studies have shown that a high consumption of fish oil or ω-3 PUFAs reduced the risk of colon, pancreatic, and endometrial cancers. The ω-3 PUFA, docosahexaenoic acid (DHA), shows anticancer activity by inducing apoptosis of some human cancer cells without toxicity against normal cells. DHA induces oxidative stress and oxidative DNA adduct formation by depleting intracellular glutathione (GSH) and decreasing the mitochondrial function of cancer cells. Oxidative DNA damage and DNA strand breaks activate DNA damage responses to repair the damaged DNA. However, excessive DNA damage beyond the capacity of the DNA repair processes may initiate apoptotic signaling pathways and cell cycle arrest in cancer cells. DHA shows a variable inhibitory effect on cancer cell growth depending on the cells’ molecular properties and degree of malignancy. It has been shown to affect DNA repair processes including DNA-dependent protein kinases and mismatch repair in cancer cells. Moreover, DHA enhanced the efficacy of anticancer drugs by increasing drug uptake and suppressing survival pathways in cancer cells. In this review, DHA-induced oxidative DNA damage, apoptotic signaling, and enhancement of chemosensitivity in cancer cells will be discussed based on recent studies.

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“…According to our data and previous publications, EPA and fish oil act primarily on tumor suppression and inflammation related to the use of 5-FU, whereas DHA plays a key role in the suppression of 5-FU induced intestinal impairment by repairing DNA. Furthermore, although our data suggests EPA and DHA have anti-apoptotic effects, which hypothetically may promote tumorgenesis, in vitro and in vivo studies have not shown any detrimental effects of EPA or DHA on chemotherapeutic agents [36][37][38].…”

Section: Discussionmentioning

confidence: 99%

The synergystic effects of omega-3 fatty acids against 5-fluorouracil-induced mucosal impairment in mice

et al. 2016

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Background: Anti-cancer pharmaceuticals frequently have adverse side effects on patients such as gastrointestinal involvement limiting their clinical applications. These effects may be controlled by nutritional interventions, however, there are few studies that have shown any mechanistic effects. In this study, we examined effects of diet enhanced with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on 5-fluorouracil (5-FU)-induced intestinal impairment and immunity in mice. Methods: C57Bl6 mice were randomized to control diet, control diet + EPA, control + DHA, control + fish oil, or diet enchanced with DHA/EPA. After seven days of each respective diet, mice, excluding those in the sham group, were treated with 10 mg/kg/day 5-FU for 7 days. The effects of 5-FU-induced impairment in the small intestine were assessed using cytokine concentrations in serum and tissue, secretory immunoglobulin (Ig) A, diamine oxidase (DAO) activity, the length of the small intestine, and the expression of apoptosis signaling genes.

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N-3 PUFAs have antiproliferative and apoptotic effects on human colorectal cancer stem-like cells in vitro

Cited by 65 publications

References 38 publications

High-saturate-fat diet delays initiation of diethylnitrosamine-induced hepatocellular carcinoma

High-saturate-fat diet delays initiation of diethylnitrosamine-induced hepatocellular carcinoma

Docosahexaenoic Acid Induces Oxidative DNA Damage and Apoptosis, and Enhances the Chemosensitivity of Cancer Cells

The synergystic effects of omega-3 fatty acids against 5-fluorouracil-induced mucosal impairment in mice

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