Role of dietary oleic acid in linoleic acid-enhanced metastasis of a mouse mammary tumor

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Abstract

We have previously shown that a high fat diet (20% w/w) containing 12% linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8% or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20% fat diets were formulated with 1%, 6%, and 12% 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12% has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1% and 6% 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12% 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12%. However, at 6% 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1% and 6% 18:2, but significantly higher levels were observed at 12% 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12% 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12% 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.

Original languageEnglish (US)
Pages (from-to)165-171
Number of pages7
JournalCancer Letters
Volume56
Issue number2
DOIs
StatePublished - 1991

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Linoleic Acid
Oleic Acid
Breast Neoplasms
Neoplasm Metastasis
Diet
High Fat Diet
Neoplasms
Growth
Fats
Cyclooxygenase Inhibitors
Eicosanoids
Indomethacin
Fatty Acids
Lung

Keywords

  • cancer
  • dietary fat
  • mammary tumor
  • metastasis

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

Cite this

Role of dietary oleic acid in linoleic acid-enhanced metastasis of a mouse mammary tumor. / Hubbard, Neil; Erickson, Kent L.

In: Cancer Letters, Vol. 56, No. 2, 1991, p. 165-171.

Research output: Contribution to journalArticle

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title = "Role of dietary oleic acid in linoleic acid-enhanced metastasis of a mouse mammary tumor",
abstract = "We have previously shown that a high fat diet (20{\%} w/w) containing 12{\%} linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8{\%} or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20{\%} fat diets were formulated with 1{\%}, 6{\%}, and 12{\%} 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12{\%} has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1{\%} and 6{\%} 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12{\%} 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12{\%}. However, at 6{\%} 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1{\%} and 6{\%} 18:2, but significantly higher levels were observed at 12{\%} 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12{\%} 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12{\%} 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.",
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AB - We have previously shown that a high fat diet (20% w/w) containing 12% linoleic acid (18:2) can significantly increase the metastasis of mammary tumor cells when compared with high fat diets that contain 8% or less 18:2 with a constant level of oleic acid (18:1). This effect may have been due to an alteration of eicosanoid metabolism because the cyclooxygenase inhibitor, indomethacin, abolished the increase. Because 18:1 may interfere with the metabolism of 18:2 to 20:4, we have now tested whether the 18:1 that supplements the 18:2 diet can have an effect on spontaneous or experimental metastasis of the line 4526 murine mammary tumor. For this, six 20% fat diets were formulated with 1%, 6%, and 12% 18:2 and either high or low levels of 18:1. Our results indicate that the amount of select fatty acids other than 18:2 at 12% has no significant effect on mouse growth, tumor growth, or tumor latency. When spontaneous metastatic burden was calculated, no significant differences between mice fed diets containing 1% and 6% 18:2 were observed. However, 4 to 5 times more of a metastatic burden was observed in mice fed diets containing 12% 18:2. No significant differences were observed between high and low 18:1 diets when the 18:2 content was 1 or 12%. However, at 6% 18:2, 18:1 significantly decreased metastatic burden. When experimental metastasis was assessed, relatively low levels of surface lung nodules were observed at 1% and 6% 18:2, but significantly higher levels were observed at 12% 18:2. The results from these experiments along with our previous findings suggest that the type of fat supplementing the 12% 18:2 diet has no effect on altering 18:2-enhanced metastasis, but that it may have an effect of lowering metastasis when the level of 18:2 is decreased. Also, because there were no differences in growth in the primary tumor, and because increased experimental metastasis was observed in mice fed 12% 18:2, increased metastasis due to high levels of 18:2 may involve that part of the metastatic cascade after which the tumor cells are released from the primary site.

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