Roles of TRPM channels in glioma.

IF 4.6 4区 医学 Q2 ONCOLOGY Cancer Biology & Therapy Pub Date : 2024-12-31 Epub Date: 2024-04-29 DOI:10.1080/15384047.2024.2338955
Zhigang Chen, Han Xie, Jun Liu, JiaJia Zhao, Ruixiang Huang, Yufei Xiang, Haoyuan Wu, Dasheng Tian, Erbao Bian, Zhang Xiong
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Abstract

Gliomas are the most common type of primary brain tumor. Despite advances in treatment, it remains one of the most aggressive and deadly tumor of the central nervous system (CNS). Gliomas are characterized by high malignancy, heterogeneity, invasiveness, and high resistance to radiotherapy and chemotherapy. It is urgent to find potential new molecular targets for glioma. The TRPM channels consist of TRPM1-TPRM8 and play a role in many cellular functions, including proliferation, migration, invasion, angiogenesis, etc. More and more studies have shown that TRPM channels can be used as new therapeutic targets for glioma. In this review, we first introduce the structure, activation patterns, and physiological functions of TRPM channels. Additionally, the pathological mechanism of glioma mediated by TRPM2, 3, 7, and 8 and the related signaling pathways are described. Finally, we discuss the therapeutic potential of targeting TRPM for glioma.

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TRPM 通道在胶质瘤中的作用。
胶质瘤是最常见的原发性脑肿瘤。尽管治疗手段不断进步,但它仍然是中枢神经系统(CNS)中侵袭性最强、最致命的肿瘤之一。胶质瘤的特点是高度恶性、异质性、侵袭性以及对放疗和化疗的高度耐受性。寻找潜在的胶质瘤新分子靶点迫在眉睫。TRPM通道由TRPM1-TPRM8组成,在细胞增殖、迁移、侵袭、血管生成等多种细胞功能中发挥作用。越来越多的研究表明,TRPM 通道可作为胶质瘤的新治疗靶点。在这篇综述中,我们首先介绍了 TRPM 通道的结构、激活模式和生理功能。此外,还介绍了由 TRPM2、3、7 和 8 介导的胶质瘤病理机制及相关信号通路。最后,我们讨论了靶向 TRPM 治疗神经胶质瘤的潜力。
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来源期刊
Cancer Biology & Therapy
Cancer Biology & Therapy 医学-肿瘤学
CiteScore
7.00
自引率
0.00%
发文量
60
审稿时长
2.3 months
期刊介绍: Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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