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The role of BCL2L13 in Glioblastoma: Turning a need into a target.
Biochemistry and Cell Biology ( IF 2.9 ) Pub Date : 2023-11-21 , DOI: 10.1139/bcb-2023-0221
Joadi Jacobs 1 , Rosa Iranpour 1 , Amir Barzegar Behrooz 1, 2 , Simone C da Silva Rosa 1 , Saeid Ghavami 1, 3, 4
Affiliation  

Glioblastoma (GBM) is the most common aggressive central nervous system (CNS) cancer. GBM has a high mortality rate, with a median survival time of 12-15 months after diagnosis. A poor prognosis and a shorter life expectancy may result from resistance to standard treatments such as radiation and chemotherapy. Temozolomide (TMZ) has been the mainstay treatment for GBM, but unfortunately, there are high rates of resistance with GBM bypassing apoptosis. A proposed mechanism for bypassing apoptosis is decreased ceramide levels, and previous research has shown that within GBM cells, BCL2L13 can inhibit ceramide synthase. This review aims to discuss the causes of resistance in GBM cells, followed by a brief description of BCL2L13 and an explanation of its mechanism of action. Further, lipids, specifically ceramide, will be discussed concerning cancer and GBM cells, focusing on ceramide synthase and its role in developing GBM. By gathering all current information on BCL2L13 and ceramide synthase, this review seeks to enable an understanding of these pieces of GBM in the hope of finding an effective treatment for this disease.

中文翻译:

BCL2L13 在胶质母细胞瘤中的作用:将需求转变为目标。

胶质母细胞瘤(GBM)是最常见的侵袭性中枢神经系统(CNS)癌症。GBM 死亡率较高,确诊后中位生存期为 12-15 个月。对放疗和化疗等标准治疗的耐药性可能导致预后不良和预期寿命缩短。替莫唑胺 (TMZ) 一直是 GBM 的主要治疗方法,但不幸的是,GBM 绕过细胞凋亡的耐药率很高。一种绕过细胞凋亡的机制是降低神经酰胺水平,之前的研究表明,在 GBM 细胞内,BCL2L13 可以抑制神经酰胺合酶。本综述旨在讨论 GBM 细胞耐药的原因,随后对 BCL2L13 进行简要描述并解释其作用机制。此外,还将讨论有关癌症和 GBM 细胞的脂质,特别是神经酰胺,重点是神经酰胺合酶及其在形成 GBM 中的作用。通过收集有关 BCL2L13 和神经酰胺合酶的所有当前信息,本综述旨在了解 GBM 的这些片段,以期找到治疗这种疾病的有效方法。
更新日期:2023-11-21
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