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Induction of MYCN-amplified neuroblastoma differentiation through NMYC suppression using PPAR-γ antagonist. PPAR-γ拮抗剂抑制NMYC诱导mycn扩增的神经母细胞瘤分化
IF 2.4
Molecular biology (Los Angeles, Calif.)
Pub Date : 2023-11-01 Epub Date: 2023-06-28 DOI: 10.3164/jcbn.23-28
Yukako Nakao-Ise, Takumi Narita, Shingo Miyamoto, Motoki Watanabe, Takuji Tanaka, Yoshihiro Sowa, Yosuke Iizumi, Mitsuharu Masuda, Gen Fujii, Yasuko Hirai, Toshimasa Nakao, Hideki Takakura, Michihiro Mutoh

Neuroblastomas are the most common extracranial solid tumors in children and have a unique feature of neuronal differentiation. Peroxisome proliferator-activated receptor (PPAR)-γ is reported to have neuroprotective effects in addition to having antitumor effects in various cancers. Thus, we aimed to clarify the role of PPAR-γ agonist and antagonist in malignant neuroblastomas, which also possess neuronal features. In MYCN-amplified neuroblastoma CHP212 cells, treatment with the PPAR-γ antagonist GW9662 induced growth inhibition in a dose-dependent manner. In addition, the PPAR-γ antagonist treatment changed cell morphology with increasing expression of the neuronal differentiation marker tubulin beta 3 (TUBB3) and induced G1 phase arrest and apoptosis in MYCN-amplified neuroblastoma. Notably, the PPAR-γ antagonist treatment significantly decreased expression of NMYC, B-cell lymphoma 2 (BCL2) and bromodomain-containing protein 4 (BRD4). It is implied that BRD4, NMYC, BCL2 suppression by the PPAR-γ antagonist resulted in cell growth inhibition, differentiation, and apoptosis induction. In our in vivo study, the PPAR-γ antagonist treatment induced CHP212 cells differentiation and resultant tumor growth inhibition. Our results provide a deeper understanding of the mechanisms of tumor cell differentiation and suggest that PPAR-γ antagonist is a new therapeutic and prevention option for neuroblastomas.

神经母细胞瘤是儿童最常见的颅外实体瘤，具有神经元分化的独特特征。据报道，过氧化物酶体增殖物激活受体(PPAR)-γ除了在各种癌症中具有抗肿瘤作用外，还具有神经保护作用。因此，我们旨在阐明PPAR-γ激动剂和拮抗剂在同样具有神经元特征的恶性神经母细胞瘤中的作用。在mycn扩增的神经母细胞瘤CHP212细胞中，PPAR-γ拮抗剂GW9662以剂量依赖的方式诱导生长抑制。此外，在mycn扩增的神经母细胞瘤中，PPAR-γ拮抗剂通过增加神经元分化标志物微管蛋白β 3 (TUBB3)的表达改变细胞形态，诱导G1期阻滞和凋亡。值得注意的是，PPAR-γ拮抗剂治疗显著降低了NMYC、b细胞淋巴瘤2 (BCL2)和含溴结构域蛋白4 (BRD4)的表达。这表明PPAR-γ拮抗剂抑制BRD4、NMYC、BCL2导致细胞生长抑制、分化和凋亡诱导。在我们的体内研究中，PPAR-γ拮抗剂治疗诱导CHP212细胞分化，从而抑制肿瘤生长。我们的研究结果为肿瘤细胞分化机制提供了更深入的了解，并表明PPAR-γ拮抗剂是神经母细胞瘤的一种新的治疗和预防选择。
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引用次数: 0
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Molecular biology (Los Angeles, Calif.)
Pub Date : 2023-09-06 DOI: 10.1134/s0026893323060031
V. Borisov, M. R. Nastasi, E. Forte
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引用次数: 0
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Molecular biology (Los Angeles, Calif.)
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Molecular biology (Los Angeles, Calif.)
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Molecular biology (Los Angeles, Calif.)
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引用次数: 0
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Molecular biology (Los Angeles, Calif.)
Pub Date : 2023-08-01 DOI: 10.1134/S0026893323040131
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Molecular biology (Los Angeles, Calif.)
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引用次数: 0
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