Fukami Kazuki, Asano Erina, Ueda Mai, Sekiguchi Fumiko, Yoshida Shigeru, Kawabata Atsufumi
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.
J Pharmacol Sci. 2017 Jan;133(1):57-60. doi: 10.1016/j.jphs.2016.12.004. Epub 2017 Jan 3.
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.
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。