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靶向癌症中的钙离子转运:接近现实还是长远展望?

Targeting Ca²⁺ transport in cancer: close reality or long perspective?

机构信息

Inserm, U1003, Laboratoire de Physiologie Cellulaire, Equipe labellisée par Ligue contre cancer, Villeneuve d'Ascq, F-59650, France.

出版信息

Expert Opin Ther Targets. 2013 Mar;17(3):225-41. doi: 10.1517/14728222.2013.741594. Epub 2013 Jan 7.

Abstract

INTRODUCTION

Cancer is caused by defects in the mechanisms underlying cell proliferation, death and migration. Calcium ions are central to all of these phenomena, serving as major signalling agents with the spatial localisation, magnitude and temporal characteristics of calcium signals ultimately determining cell's fate. The transformation of a normal cell into a malignant derivative is associated with a major rearrangement of Ca(2+) pumps, Na/Ca exchangers and Ca(2+) channels, which leads to enhanced proliferation and invasion under compromised/impaired ability to die.

AREAS COVERED

This paper examines the changes in Ca(2+) signalling and the mechanisms that underlie the passage from normal to pathological cell growth and death control. Understanding these changes and identifying the molecular players involved provide new perspectives for cancer treatment.

EXPERT OPINION

Despite compelling evidence that the disruption of Ca(2+) homeostasis in cancer cells leads to the promotion of certain malignant phenotypes as well as the identification of key Ca(2+)-transporting molecules whose altered expression and/or function underlies pathological changes, the therapeutic utilisation of these findings for cancer treatment is still at its infancy. However, the rapid development of the field warrants the development of improved molecular Ca(2+) transport-targeting tools for cancer diagnosis and treatment.

摘要

简介

癌症是由细胞增殖、死亡和迁移机制中的缺陷引起的。钙离子是所有这些现象的核心,作为主要的信号分子,钙离子信号的空间定位、幅度和时间特征最终决定了细胞的命运。正常细胞向恶性衍生物的转化与钙(Ca 2+)泵、钠/钙交换器和 Ca 2+通道的重大重排有关,这导致在死亡能力受损/受损的情况下增强增殖和侵袭。

涵盖领域

本文研究了 Ca 2+信号转导的变化以及从正常到病理性细胞生长和死亡控制的转变背后的机制。了解这些变化并确定涉及的分子参与者为癌症治疗提供了新的视角。

专家意见

尽管有确凿的证据表明,癌细胞中 Ca 2+稳态的破坏会促进某些恶性表型的出现,并且确定了关键的 Ca 2+转运分子,其异常表达和/或功能是病理性变化的基础,但这些发现对癌症治疗的治疗应用仍处于起步阶段。然而,该领域的快速发展需要开发用于癌症诊断和治疗的改进的分子 Ca 2+转运靶向工具。

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