Abstract
Sesamolin is one of the lignans derived from sesame oil. It has demonstrated significant antioxidant, anti-aging, and anti-mutagenic properties. It also reportedly augments natural killer (NK) cell lysis activity. We previously reported that sesamolin also exerts anticancer effects in vitro and induces enhanced NK cell cytolytic activity against tumor cells. Herein, we aimed to determine the mechanism by which sesamolin prevents and retards tumorigenesis in BALB/c mouse models of leukemia induced by murine (BALB/c) myelomonocytic leukemia WEHI-3B cells. Banded neutrophils, myeloblasts, and monocytic leukemic cells were more abundant in the leukemia model than in normal mice. Sesamolin decreased the number of leukemic cells by almost 60% in the leukemia model mice in vivo; additionally, sesamolin and the positive control drug, vinblastine, similarly hindered neoplastic cell proliferation. Spleen samples were ~ 4.5-fold heavier in leukemic mice than those obtained from normal mice, whereas spleen samples obtained from leukemic mice treated with sesamolin had a similar weight to those of normal mice. Moreover, sesamolin induced a twofold increase in the cytotoxic activity of leukemic mouse NK cells against WEHI-3B cells. These results indicated that sesamolin exerts anti-leukemic effects in vivo.
Highlights
Cancer is generally defined as atypical cell proliferation, and the hallmarks of tumor development comprise insensitivity to anti-growth signals, metastasis, apoptotic evasion, unlimited replicative potential, and sustained angiogenesis [1, 2]
Our results indicated that the increased sensitivity of sesamolin-treated myeloma cells to natural killer (NK) cell lysis is caused by heightened NKG2D ligand expression on the surface of myeloma cells, resulting from a more robust ERK signaling pathway [9]
We previously showed that sesamolin exerts anticancer activity in vitro [9]
Summary
Cancer is generally defined as atypical cell proliferation, and the hallmarks of tumor development comprise insensitivity to anti-growth signals, metastasis, apoptotic evasion, unlimited replicative potential, and sustained angiogenesis [1, 2]. The most common cause of cancer is chronic inflammation [3], during which the immune system is tasked with releasing protective agents, such as reactive oxygen species and nitric oxide, to counter pathogens [4]. These agents disrupt the DNA repair mechanisms, which can result in DNA mutations [3]. We disclosed that sesamolin stimulates NK cell cytolytic activity via phosphorylation of the p38, ERK1/2 and JNK pathways [10] These findings indicated that sesamolin exerts therapeutic effects against tumors.
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