Chronic
inflammation is one of the foremost risk factors for different types of
malignancies, including
breast cancer. Additional risk factors of this pathology in postmenopausal women are
weight gain,
obesity,
estrogen secretion, and an imbalance in the production of
adipokines, such as
leptin and
adiponectin. Various signaling products of
transcription factor,
nuclear factor-kappaB, in particular inflammatory
eicosanoids,
reactive oxygen species (ROS), and
cytokines, are thought to be involved in chronic
inflammation-induced
cancer. Together, these key components have an influence on inflammatory reactions in malignant tissue damage when their levels are deregulated endogenously.
Prostaglandins (PGs) are well recognized in
inflammation and
cancer, and they are solely biosynthesized through
cyclooxygenases (COXs) from
arachidonic acid. Concurrently, ROS give rise to bioactive
isoprostanes from
arachidonic acid precursors that are also involved in acute and chronic
inflammation, but their specific characteristics in
breast cancer are less demonstrated. Higher
aromatase activity, a
cytochrome P-450 enzyme, is intimately connected to
tumor growth in the breast through
estrogen synthesis, and is interrelated to COXs that catalyze the formation of both inflammatory and anti-inflammatory PGs such as
PGE(2),
PGF(2α),
PGD(2), and PGJ(2) synchronously under the influence of specific mediators and downstream
enzymes. Some of the latter compounds upsurge the intracellular cyclic
adenosine monophosphate concentration and appear to be associated with
estrogen synthesis. This review discusses the role of COX- and ROS-catalyzed
eicosanoids and
adipokines in
breast cancer, and therefore ranges from their molecular mechanisms to clinical aspects to understand the impact of
inflammation.