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高糖诱导神经内分泌样分化的人前列腺癌细胞中Ca3.2 T型钙通道的N-糖基化介导的功能上调和过表达。

High glucose induces N-linked glycosylation-mediated functional upregulation and overexpression of Ca3.2 T-type calcium channels in neuroendocrine-like differentiated human prostate cancer cells.

作者信息

Fukami Kazuki, Asano Erina, Ueda Mai, Sekiguchi Fumiko, Yoshida Shigeru, Kawabata Atsufumi

机构信息

Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University (Formerly Kinki University), Higashi-Osaka 577-8502, Japan.

Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashi-Osaka 577-8502, Japan.

出版信息

J Pharmacol Sci. 2017 Jan;133(1):57-60. doi: 10.1016/j.jphs.2016.12.004. Epub 2017 Jan 3.

Abstract

Given that Ca3.2 T-type Ca channels were functionally regulated by asparagine (N)-linked glycosylation, we examined effects of high glucose on the function of Ca3.2, known to regulate secretory function, in neuroendocrine-like differentiated prostate cancer LNCaP cells. High glucose accelerated the increased channel function and overexpression of Ca3.2 during neuroendocrine differentiation, the former prevented by enzymatic inhibition of N-glycosylation and cleavage of N-glycans. Hyperglycemia thus appears to induce N-linked glycosylation-mediated functional upregulation and overexpression of Ca3.2 in neuroendocrine-like differentiated prostate cancer cells.

摘要

鉴于Ca3.2 T型钙通道受天冬酰胺(N)-连接糖基化的功能调控,我们研究了高糖对神经内分泌样分化的前列腺癌LNCaP细胞中Ca3.2功能的影响,已知Ca3.2可调节分泌功能。高糖加速了神经内分泌分化过程中Ca3.2通道功能的增强和其过表达,前者可通过N-糖基化的酶抑制作用和N-聚糖的切割来阻止。因此,高血糖似乎在神经内分泌样分化的前列腺癌细胞中诱导了N-连接糖基化介导的Ca3.2功能上调和过表达。

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