The role of tumor suppressor of resveratrol and prednisolone by downregulation of YKL‐40 expression in CCRF‐CEM cell line

Abstract

Background: Acute lymphoblastic leukemia (ALL) is characterized by excessive accumulation of lymphoblast and progenitors. Leukemia is the most common cancer in children and ALL is the most common subtype. Many studies have shown that the YKL-40 gene is one of the most widely expressed genes in tumors, including leukemia, but not in healthy blood cells. Clinical studies have shown that serum YKL-40 levels have a positive correlation with tumor expansion, in addition to being a prognostic agent independent of a short relapse-free interval, as well as a brief overall survival in patients with various cancers. The previous study shows that YKL-40 is closely related to the degree of pathology or degree of human leukemia pathology and plays an important role in cell proliferation. Hence, the YKL-40 can be an attractive target in designing anticancer therapies. Methods: CCRF-CEM cells were treated with resveratrol and prednisolone. For analysis of YKL-40 expression changes under medication, real-time polymerase chain reaction (PCR) and Western blot techniques were used at resonating intervals of 24 and 48 hours. Results: The effect of 15, 50, and 100 μM resveratrol and 700 μM of prednisolone on CCRF-CEM cells reduced YKL-40. The YKL-40 gene was quantitatively measured using RT-PCR. The Western blot method was used to evaluate changes in the expression of YKL-40 protein. Conclusion: In this study, we first evaluated YKL-40 expression and resveratrol and prednisolone effect on YKL-40 in ALL. This finding supports the idea of targeting YKL-40 as a new drug treatment of ALL and extends the use of resveratrol in antileukemia research. K E Y W O R D S acute lymphoblastic leukemia, gene expression, prednisolone, resveratrol, YKL-40 gene

Recent advances in pre-conditioned mesenchymal stem/stromal cell (MSCs) therapy in organ failure; a comprehensive review of preclinical studies

“…These engineered MSCs also decreased the apoptotic cell numbers in the infarcted area and caused the reduction of left ventricular remodeling in vivo [ 118 ]. Besides, another study on a mouse model of heart failure demonstrated that overexpression of anti-fibrotic substances, adrenomedullin (ADM), dramatically improved heart function, decreased fibrotic area, and decreased MMP-2 expression [ 119 – 122 ]. The ADM-MSC-treated group also shows markedly higher MSCs survival after transplantation.…”