乳腺癌和妇科癌症的通道病变

Chandana Yesudas, Uma Maheshwari, Illakkiam Devaraj
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摘要

越来越多的证据表明,离子通道在细胞增殖、迁移、凋亡和分化中发挥着重要作用。在妇科癌症的许多研究工作表明,离子通道参与异常肿瘤生长,离子通道的上调或下调导致肿瘤生长停滞。通道病是一组不同的离子通道遗传突变,导致生物物理特性的改变。在正常细胞中,细胞生长和细胞死亡之间存在切换,这显然取决于不同离子通道的时间组织和大小。需要特异性离子通道阻断剂,其可以消除癌症细胞的细胞机制。通常,离子通道对癌症的影响取决于离子通道激活的幅度和时间组织以及其他信号机制的活性。膜蛋白负责离子通道中的离子稳态。由于癌症可能与离子通道的生物物理性质改变有关,癌症中不同离子通道的边界背景似乎是绝对合适的。肿瘤治疗领域正在迅速扩展,了解癌症发展的病理生理机制使研究人员能够更好地诊断和开发癌症的治疗方案。本文综述了离子通道在乳腺癌症和其他妇科癌症(包括卵巢癌症和癌症)中的作用,以及它们如何促进肿瘤的发展。
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Channelopathies in Breast Cancer and Gynecological Cancers
Increasing evidence shows that ion channels play a significant role in cell proliferation, migration, apoptosis and differentiation. Many research works in gynecological cancer suggest that ion channels are involved in aberrant tumor growth and upregulation or downregulation of ion channels results in tumor growth arrest. Channelopathies are a diverse set of inherited mutations of ion channels that result in altered biophysical properties. In normal cells, there is a switch between cell growth and cell death which apparently depend upon the temporal organization and magnitude of different ion channels. There is a need for specific ion channel blockers which can abrogate the cellular mechanism of the cancer cell. Typically the impact of ion channels on cancer depends upon the magnitude and temporal organization of the ion channel activation and the activity of other signaling mechanisms. Membrane proteins are responsible for ionic homeostasis in ion channels. As cancer can be linked with the altered biophysical properties of ion channels a border context of different ion channels in cancer seems absolutely appropriate. The field of onco-channelopathies is rapidly expanding and understanding the pathophysiological mechanisms underlying the development of cancer enables researchers to better diagnose and develop treatment options for cancer. This review focuses on the role of ion channels in breast cancer and other gynecological cancers including ovarian cancer and cervical cancer, and how they contribute to tumor development.
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