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3. Loss of natural killer T cells promotes pancreatic cancer in LSL-KrasG12D/+ mice.

Author

Janakiram, Naveena B., Mohammed, Altaf, Bryant, Taylor, Ritchie, Rebekah, Stratton, Nicole, Jackson, Lydgia, Lightfoot, Stan, Benbrook, Doris M., Asch, Adam S., Lang, Mark L., and Rao, Chinthalapally V.

Subjects
KILLER cells, CANCER invasiveness, PROSTAGLANDIN E1, LIPOXYGENASES, PANCREATIC intraepithelial neoplasia
Abstract

The role of the unique T-cell population, natural killer T ( NKT) cells, which have similar functions to NK cells in pancreatic cancer ( PC), is not yet evaluated. To address the regulatory roles of NKT cells on tumour progression through tumour-associated macrophages ( TAM) and their production of microsomal prostaglandin E synthase-1 ( mPGES-1) and 5-lipoxygenase (5- LOX) in (Kras)-driven pancreatic tumour ( KPT) progression, we crossed CD1d−/− mice deficient in both invariant and variant NKT cells with the KrasG12D mice. Loss of NKT cells significantly increased pancreatic intraepithelial neoplasia (Pan IN) lesions and also increased 5- LOX and mPGES-1 expression in M2-type macrophages and cancer stem-like cells in pancreatic tumours. Pharmacological inhibition of mPGES-1 and 5- LOX in M2 macrophages with specific inhibitor YS-121 in KPT- CD1d−/− mice decreased Pan IN lesions and suppressed tumour growth in association with elevated levels of active CD8a cells. Hence, NKT cells regulate PC by modulating TAMs (M2) through mPGES-1 and 5- LOX; and the absence of NKT cells leads to aggressive development of PC. [ABSTRACT FROM AUTHOR]

Published
2017
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4. Loss of natural killer T cells promotes pancreatic cancer in LSL-Kras G12D/+ mice.

Author

Janakiram NB, Mohammed A, Bryant T, Ritchie R, Stratton N, Jackson L, Lightfoot S, Benbrook DM, Asch AS, Lang ML, and Rao CV

Subjects
Animals, Antigens, CD1d genetics, Arachidonate 5-Lipoxygenase immunology, Arachidonate 5-Lipoxygenase metabolism, CD8 Antigens immunology, CD8 Antigens metabolism, Carcinoma in Situ genetics, Carcinoma in Situ metabolism, Carcinoma in Situ prevention & control, Cell Proliferation, Disease Progression, Genes, ras, Genetic Predisposition to Disease, Humans, Lipoxygenase Inhibitors pharmacology, Macrophages drug effects, Macrophages metabolism, Mice, Inbred C57BL, Mice, Knockout, Natural Killer T-Cells metabolism, Neoplastic Stem Cells immunology, Neoplastic Stem Cells pathology, Pancreatic Neoplasms genetics, Pancreatic Neoplasms metabolism, Pancreatic Neoplasms prevention & control, Phenotype, Prostaglandin-E Synthases antagonists & inhibitors, Prostaglandin-E Synthases immunology, Prostaglandin-E Synthases metabolism, Signal Transduction, T-Lymphocytes, Regulatory immunology, T-Lymphocytes, Regulatory metabolism, Time Factors, Carcinoma in Situ immunology, Macrophages immunology, Natural Killer T-Cells immunology, Pancreatic Neoplasms immunology
Abstract

The role of the unique T-cell population, natural killer T (NKT) cells, which have similar functions to NK cells in pancreatic cancer (PC), is not yet evaluated. To address the regulatory roles of NKT cells on tumour progression through tumour-associated macrophages (TAM) and their production of microsomal prostaglandin E synthase-1 (mPGES-1) and 5-lipoxygenase (5-LOX) in (Kras)-driven pancreatic tumour (KPT) progression, we crossed CD1d -/- mice deficient in both invariant and variant NKT cells with the Kras G12D mice. Loss of NKT cells significantly increased pancreatic intraepithelial neoplasia (PanIN) lesions and also increased 5-LOX and mPGES-1 expression in M2-type macrophages and cancer stem-like cells in pancreatic tumours. Pharmacological inhibition of mPGES-1 and 5-LOX in M2 macrophages with specific inhibitor YS-121 in KPT-CD1d -/- mice decreased PanIN lesions and suppressed tumour growth in association with elevated levels of active CD8a cells. Hence, NKT cells regulate PC by modulating TAMs (M2) through mPGES-1 and 5-LOX; and the absence of NKT cells leads to aggressive development of PC., (© 2017 John Wiley & Sons Ltd.)

Published
2017
Full Text
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