Induction of Apoptosis in Human Pancreatic Cancer Cells by Docosahexaenoic Acid

Merendino, Nicolò; Molinari, Romina; Loppi, Barbara; Pessina, G; D'Aquino, Massimo; Tomassi, G.; Velotti, Francesca

doi:10.1196/annals.1299.143

Cited by 26 publications

(18 citation statements)

References 14 publications

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“…Both ROS and RNS induce DNA damage and DNA strand breaks. Merendino et al [35] showed that DHA induced oxidative stress by depleting intracellular glutathione (GSH) in Paca-44 pancreatic cancer cells. They suggested that GSH depletion occurred via active GSH extrusion in cancer cells, since the inhibition of GSH efflux by treatment with the specific inhibitors of carrier-mediated GSH extrusion, cystathionine or methionine, completely reversed the apoptosis.…”

Section: Dha Induces Oxidative Stress and Oxidative Dna Damage To mentioning

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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Section: Dha Induces Oxidative Stress and Oxidative Dna Damage To mentioning

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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“…However, even though limited in number, the available studies strongly suggest the efficacy of these nutraceutical compounds against the growth of several other cancer cells, including those of pancreatic [116,117], lung [32], prostatic [118][119][120], hepatic [63,121,122] and nervous [123] origin.…”

Section: Cancer Cells Of Other Originmentioning

confidence: 99%

Differential Anti-Cancer Effects of Purified EPA and DHA and Possible Mechanisms Involved

Serini¹,

Fasano²,

Piccioni³

et al. 2011

CMC

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As the concepts of pharmaconutrition are receiving increasing attention, it seems essential to clearly assess the effects of specific dietary compounds in specific groups of patients or clinical conditions. We are herein interested in better defining the differential anti-neoplastic effects of the two major n-3 long chain polyunsaturated fatty acids present in fish oil, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The efficiency of these fatty acids represents a subject of intense interest and debate, and whereas plenty of preclinical studies have strongly demonstrated their preventive and therapeutic effect in different kinds of cancers, the results of the epidemiologic studies are still controversial, and only a few trials have been performed. It has been reported that EPA and DHA may act either through the same or different mechanisms, thus suggesting that a differential efficacy could exist. At present, however, this point has not been clarified, although its better comprehension would allow a more proper and effective use of these fatty acids in the human interventional studies. In an attempt to elucidate this aspect we have herein analyzed the data obtained in the studies which have directly compared the antitumor effects of separate treatments with EPA or DHA. Most of the in vitro data indicate DHA as the more powerful antineoplastic agent. However, an equivalent efficiency of EPA and DHA is suggested by the few in vivo studies. Possible reasons for this discrepancy are discussed and pathways of cell growth that could be differentially influenced by EPA and DHA are described.

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“…These names reflect the type of cell from 260 which the cancer developed [49]. pancreatic cancer and assuming a causality between dietary con-289 tent of n-6 PUFAs and carcinogenesis [55,56]. Thus an increased 290 incidence of pancreatic cancer and liver metastasis was achieved 291 by a dietary modification [55].…”

Section: Introductionmentioning

confidence: 98%

“…pancreatic cancer and assuming a causality between dietary con-289 tent of n-6 PUFAs and carcinogenesis [55,56]. Thus an increased 290 incidence of pancreatic cancer and liver metastasis was achieved 291 by a dietary modification [55]. While CLA is regarded as an essen- Liver cancer or hepatic cancer is a cancer that originates in the 329 liver [54].…”

Section: Introductionmentioning

confidence: 99%

Biological effects of conjugated linoleic acid on obesity-related cancers

Moon

2014

Chemico-Biological Interactions

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Induction of Apoptosis in Human Pancreatic Cancer Cells by Docosahexaenoic Acid

Cited by 26 publications

References 14 publications

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

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

Differential Anti-Cancer Effects of Purified EPA and DHA and Possible Mechanisms Involved

Biological effects of conjugated linoleic acid on obesity-related cancers

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